Journal articles on the topic 'HepG2 cells'
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1
Sary, Hanan G., Nahla A. Ayoub, Abdel Nasser B. Singab, Mickey Vinodh, and Khaled Y. Orabi. "ISOLATION OF BIOACTIVE COMPOUNDS FROM CENTAUREA AEGYPTIACA." International Journal of Pharmacy and Pharmaceutical Sciences 10, no. 4 (April 1, 2018): 1. http://dx.doi.org/10.22159/ijpps.2018v10i4.17528.
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Objective: In a previous study, Centaurea aegyptiaca ethanol and ethyl acetate extracts showed potent cytotoxic effects against laryngeal (HEP2) and hepatic (HEPG2) carcinoma cell lines. Additionally, two novel compounds were isolated and identified. The aim of this study is to continue isolating and identifying another compound (s) that may, also, be responsible for this potent biological activity.Methods: C. aegyptiaca dried aerial parts were extracted with ethanol and ethyl acetate. Both extracts were chromatographed separately to afford seven guaianolides that were identified using different spectroscopic methods. Moreover, compounds 1-7 were evaluated for their cytotoxicity (IC50, µM) against HEP2 and HEPG2 cells in comparison to the normal fibroblasts (BHK) using sulforhodamine B assay. Doxorubicin was used as a positive control.Results: Seven sesquiterpene lactones, centaurepensin, also known as chlorohyssopifolin A (1), 8α-hydroxy-11α, 13-dihydrozaluzanin C (2), chlorohyssopifolin B (3), desacylcynaropicrin (4), chlorohyssopifolin C, acroptilin (5), subluteolide (6), and solstitiolide (7) were isolated from C. aegyptiaca extracts and identified. This is the first report on the occurrence of 2, 4, 5 and 6 in C. aegyptiaca. Compounds 1-4 and 6 exhibited selective cytotoxic effects against HEP2 and HEPG2 cells. However, compounds 1 and 7 showed the highest activities against HEP2 with IC50 values of 10.6±0.02 and 10.9±0.03 µM, respectively. Moreover, compound 3 was the most potent one against HEPG2 cells with IC50value of 13.8±0.05 µM.Conclusions: Chemical investigation of C. aegyptiaca ethanol and ethyl acetate extracts led to the isolation and identification of seven guaianolides. These compounds exhibited good cytotoxic activities against HEP2 and HEPG2 cell lines.
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Pang, Ye-Bin, Jian He, Bi-Yu Cui, Sheng Xu, Xi-Lei Li, Man-Ya Wu, Rong Liang, et al. "A Potential Antitumor Effect of Dendritic Cells Fused with Cancer Stem Cells in Hepatocellular Carcinoma." Stem Cells International 2019 (April 1, 2019): 1–10. http://dx.doi.org/10.1155/2019/5680327.
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HCC stem cells were reported as posttreatment residual tumor cells that play a pivotal role in tumor relapse. Fusing dendritic cells (DCs) with tumor cells represents an ideal approach to effectively activate the antitumor immunity in vivo. DC/HCC stem cell vaccine provides a potential strategy to generate polyclonal immune response to multiple tumor stem cell antigens including those yet to be unidentified. To assess the potential capacity of DC/HCC stem cell vaccines against HCC, CD90+HepG2 cells were sorted from the HCC cell line HepG2. DC and CD90+HepG2 and DC and HepG2 fused cells were induced by polyethylene glycol (PEG). The influence of fusion cells on proliferation and immunological function transformation of lymphocytes was assessed by FCM and ELISA assay, respectively. The cytotoxicity assay of specific fusion cell-induced CTLs against HepG2 was conducted by CytoTox 96 Non-Radioactive Cytotoxicity Assay kit in vitro. At last, the prevention of HCC formation in vivo was described in a mouse model. The results of FCM analysis showed that the proportion of CD90+HepG2 cells in the spheral CD90+HepG2 enriched by suspension sphere culture was ranging from 98.7% to 99.5%, and 57.1% CD90+HepG2/DC fused cells were successfully constructed. The fusion cells expressed a higher level of costimulatory molecules CD80, CD83, CD86, and MHC-I and MHC-II molecules HLA-ABC and HLA-DR than did immature DCs (P<0.05). And the functional analysis of fusion cell-induced CTLs also illustrated that CD90+HepG2/DC fusion cells showed a greater capacity to activate proliferation of lymphocytes in vitro (P<0.05). The CD90+HepG2/DC-activated CTLs had a specific killing ability against CD90+HepG2 cells in vivo. These results suggested that CD90+HepG2/DC fusion cells could efficiently stimulate T lymphocytes to generate specific CTLs targeting CD90+HepG2 cells. It might be a promising strategy of immunotherapy for HCC.
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Choi, Hyo-Kyoung, and Min-Yu Chung. "Isoeugenol Inhibits PCSK9 in HepG2 Cells." Journal of the Korean Society of Food Science and Nutrition 49, no. 9 (September 30, 2020): 919–24. http://dx.doi.org/10.3746/jkfn.2020.49.9.919.
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Lee, Junmin, Aly Ung, Hanjun Kim, KangJu Lee, Hyun-Jong Cho, Praveen Bandaru, Samad Ahadian, Mehmet R. Dokmeci, and Ali Khademhosseini. "Engineering liver microtissues to study the fusion of HepG2 with mesenchymal stem cells and invasive potential of fused cells." Biofabrication 14, no. 1 (November 30, 2021): 014104. http://dx.doi.org/10.1088/1758-5090/ac36de.
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Abstract Increasing evidence from cancer cell fusion with different cell types in the tumor microenvironment has suggested a probable mechanism for how metastasis-initiating cells could be generated in tumors. Although human mesenchymal stem cells (hMSCs) have been known as promising candidates to create hybrid cells with cancer cells, the role of hMSCs in fusion with cancer cells is still controversial. Here, we fabricated a liver-on-a-chip platform to monitor the fusion of liver hepatocellular cells (HepG2) with hMSCs and study their invasive potential. We demonstrated that hMSCs might play dual roles in HepG2 spheroids. The analysis of tumor growth with different fractions of hMSCs in HepG2 spheroids revealed hMSCs’ role in preventing HepG2 growth and proliferation, while the hMSCs presented in the HepG2 spheroids led to the generation of HepG2-hMSC hybrid cells with much higher invasiveness compared to HepG2. These invasive HepG2-hMSC hybrid cells expressed high levels of markers associated with stemness, proliferation, epithelial to mesenchymal transition, and matrix deposition, which corresponded to the expression of these markers for hMSCs escaping from hMSC spheroids. In addition, these fused cells were responsible for collective invasion following HepG2 by depositing Collagen I and Fibronectin in their surrounding microenvironment. Furthermore, we showed that hepatic stellate cells (HSCs) could also be fused with HepG2, and the HepG2-HSC hybrid cells possessed similar features to those from HepG2-hMSC fusion. This fusion of HepG2 with liver-resident HSCs may propose a new potential mechanism of hepatic cancer metastasis.
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Zhou, Shuping, Yongfang Ma, Xueke Liu, Pan Yu, Ning Huang, Li Song, Ruyue Xu, Zhen Huo, Tao Zhu, and Xiaolong Tang. "Targeted Delivery of Glypican 3 (GPC3) Antibody-Modified MicroRNA (miR let-7b-5p) Polymer Nanoparticles to Sorafenib-Resistant Hepatsocellular Carcinoma Cells." Journal of Biomedical Nanotechnology 17, no. 4 (April 1, 2021): 677–90. http://dx.doi.org/10.1166/jbn.2021.3033.
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The miR let-7b-5p (a kind of microRNAs) has many pathophysiological regulation effects, including human hepatocellular carcinoma (HCC) pathogenesis. This study investigated whether nanoparticle-mediated miR let-7b-5p could jointly enhance the therapeutic effect of sorafenib on HCC by inhibiting the proliferation of HCC cells, inducing apoptosis, and reversing drug resistance. We evaluated the level of miR let-7b-5p in sorafenib-resistant HepG2 cells (HepG2R) and HepG2 HCC cells by qRT-PCR and analyzed the biological effects of hepatocellular carcinoma treated with sorafenib with miR let-7b-5p, and further studied the toxicity of nanoparticles (Ab-miR-NPs) that deliver miR let-7b-5p mimics and target GPC3 on the surface of hepatocellular carcinoma cells. Results showed that, in HepG2 cells, the expression level of miR let-7b-5p was significantly higher than that in HepG2R cells. Targeted nanoparticle Ab-miR-NPs mediated the delivery of miR let-7b-5p to the HCC cytoplasm and released miRNA after being broken down, down-regulating the expression of IGF1R and inhibiting AKT/mTOR and Ras/Raf signal transmission. Ab-miR-NPs not only enhanced the proliferation of sorafenib in cultured HepG2R cells and induced cell apoptosis efficiency, but they also improved the anti-tumor activity in the mouse models. These results indicated that GPC3 antibody-modified PLGA-PLL (polylactic acid-glycolic acetic copolymer grafted hyper-branched polylysine) loaded miR let-7b-5p polymer nanoparticles combined with sorafenib may be a new treatment strategy for HCC resistant to sorafenib.
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Chang, Xiaomin, Xuerong Zhao, Jianping Wang, Shi Ding, Lijun Xiao, Enhong Zhao, and Xin Zheng. "Effect of Hsp90 Inhibitor KW-2478 on HepG2 Cells." Anti-Cancer Agents in Medicinal Chemistry 19, no. 18 (February 7, 2020): 2231–42. http://dx.doi.org/10.2174/1871520619666191023094610.
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Objective: The objectives of this study were to investigate the effects of proliferation, apoptosis, cell cycle, invasion, and senescence of KW-2478 on HepG2 cells, and to explore the related mechanism of apoptosis and the cell cycle. Methods: HepG2 cells (hepatocellular carcinoma cells) were cultured with KW-2478, at different doses and for different times, in vitro. The MTT assay was used to detect the effect of KW-2478 on proliferation of HepG2 cells. Flow cytometry was used to determine the effects of KW-2478 on the cell cycle and apoptosis of HepG2 cells. The Transwell assay was used to determine the effect of KW-2478 on cell invasion. The β-galactosidase assay tested the effect of low-dose KW-2478 on the senescence of HepG2 cells. Western blotting and the quantitative polymerase chain reaction were used respectively to assess changes in protein and mRNA levels of related factors in HepG2 cells after the KW-2478 treatment. Results: KW-2478 significantly inhibited proliferation of HepG2 cells. KW-2478 induced apoptosis and cell cycle arrest of HepG2 cells, and inhibited the invasion of HepG2 cells; low dose KW-2478 promoted HepG2 senescence. Conclusions: KW-2478 inhibited the proliferation of HepG2 cells, induced apoptosis and cell cycle arrest, inhibited invasion, and promoted senescence. KW-2478 affected the expression of related factors in the mitochondrial apoptotic signaling and cell cycle-related regulatory pathways. KW-2478 downregulated the expression of STAT3, which is a key factor in the JAK-STAT pathway, indicating that KW-2478 may affect the function of HepG2 cells by downregulating STAT3.
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Abdel Aziz, Mohamed Talaat, Hussien Mostafa Khaled, Ali El Hindawi, Nagwa Kamal Roshdy, Laila A. Rashed, Dina Sabry, Amira A. Hassouna, Fatma Taha, and Walaa Ibrahim Ali. "Effect of Mesenchymal Stem Cells and a Novel Curcumin Derivative on Notch1 Signaling in Hepatoma Cell Line." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/129629.
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This study was conducted to evaluate the effect of mesenchymal stem cells (MSCs) and a novel curcumin derivative (NCD) on HepG2 cells (hepatoma cell line) and to investigate their effect on Notch1 signaling pathway target genes. HepG2 cells were divided into HepG2 control group, HepG2 cells treated with MSC conditioned medium (MSCs CM), HepG2 cells treated with a NCD, HepG2 cells treated with MSCs CM and NCD, and HepG2 cells treated with MSCs CM (CM of MSCs pretreated with a NCD). Expression of Notch1, Hes1, VEGF, and cyclin D1 was assessed by real-time, reverse transcription-polymerase chain reaction (RT-PCR) in HepG2 cells. In addition, HepG2 proliferation assay was performed in all groups. Notch1 and its target genes (Hes1 and cyclin D1) were downregulated in all treated groups with more suppressive effect in the groups treated with both MSCs and NCD. Also, treated HepG2 cells showed significant decrease in cell proliferation rate. These data suggest that modulation of Notch1 signaling pathway by MSCs and/or NCD can be considered as a therapeutic target in HCC.
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Negoro, Ryosuke, Mitsuki Tasaka, Sayaka Deguchi, Kazuo Takayama, and Takuya Fujita. "Generation of HepG2 Cells with High Expression of Multiple Drug-Metabolizing Enzymes for Drug Discovery Research Using a PITCh System." Cells 11, no. 10 (May 18, 2022): 1677. http://dx.doi.org/10.3390/cells11101677.
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HepG2 cells are an inexpensive hepatocyte model that can be used for repeated experiments, but HepG2 cells do not express major cytochrome P450s (CYPs) and UDP glucuronosyltransferase family 1 member A1 (UGT1A1). In this study, we established CYP3A4–POR–UGT1A1–CYP1A2–CYP2C19–CYP2C9–CYP2D6 (CYPs–UGT1A1) knock-in (KI)-HepG2 cells using a PITCh system to evaluate whether they could be a new hepatocyte model for pharmaceutical studies. To evaluate whether CYPs–UGT1A1 KI-HepG2 cells express and function with CYPs and UGT1A1, gene expression levels of CYPs and UGT1A1 were analyzed by using real-time PCR, and metabolites of CYPs or UGT1A1 substrates were quantified by HPLC. The expression levels of CYPs and UGT1A1 in the CYPs–UGT1A1 KI-HepG2 cells were comparable to those in primary human hepatocytes (PHHs) cultured for 48 h. The CYPs and UGT1A1 activity levels in the CYPs–UGT1A1 KI-HepG2 cells were much higher than those in the wild-type (WT)-HepG2 cells. These results suggest that the CYPs–UGT1A1 KI-HepG2 cells expressed functional CYPs and UGT1A1. We also confirmed that the CYPs–UGT1A1 KI-HepG2 cells were more sensitive to drug-induced liver toxicity than the WT-HepG2 cells. CYPs–UGT1A1 KI-HepG2 cells could be used to predict drug metabolism and drug-induced liver toxicity, and they promise to be a helpful new hepatocyte model for drug discovery research.
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Tian, Sha, Zhuo Liu, Qing Zhou, Ruoxia Wu, Xiaodi Huang, Zicheng Liang, Zhen Zhang, and Xuefei Tian. "Upregulation of MiR-340-5p Reverses Cisplatin Sensitivity by Inhibiting the Expression of CDK6 in HepG2 Cells." Folia Biologica 69, no. 2 (July 13, 2021): 57–66. http://dx.doi.org/10.3409/fb_69-2.08.
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Cisplatin (CDDP) has been successfully used in chemotherapy for liver cancer. However, the development of CDDP resistance in HepG2 cells usually leads to relapse and a worsening prognosis. MiR-340-5p has attracted much attention because of its ability to affect cell resistance. This project is intended to explore the role of miR-340-5p and CDK6 in CDDP-R HepG2 cells and provide new ideas for the treatment of liver cancer. A dual-luciferase reporter assay was used to confirm the targeting relationship between miR-340-5p and CDK6. We constructed a CDDP-resistant model of HepG2 cells to examine the effect of miR-340-5p on the drug sensitivity of HepG2 cells. CDDP-R HepG2 cells were transfected with miR-340-5p overexpression plasmid and CDK6 silencing plasmid. QRT-PCR was used to detect the expression of miR-340-5p and CDK6. A western blot was performed to determine the expression of CDK6, CyclinD1, and CyclinD2. CCK-8, flow cytometry, TUNEL and Clonogenic assays were also carried out to detect CDDP-R HepG2 cells. There is a targeting relationship between miR-340-5p and CDK6. The drug resistance of CDDP-R HepG2 cells was significantly higher than that of CDDP-S HepG2 cells. CDDP-R HepG2 cells transfected with both miR-340-5p overexpressing plasmid and CDK6 silencing plasmid showed a lower proliferation ability, cell cycle arrest in the G0/G1 phase, and lower drug resistance compared with single CDDP-R HepG2 cells. Overexpression of miR-340-5p aggravated CDDP-R HepG2 cells' apoptosis and inhibited cell viability. Overexpression of miR-340-5p could reverse the sensitivity of HepG2 cells to CDDP by inhibiting the expression of CDK6 in HepG2 cells.
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Alburae, Najla Ali, and Afrah Eltayeb Mohammed. "Antiproliferative effect of the Red Sea cone snail, Conus geographus." Tropical Journal of Pharmaceutical Research 19, no. 3 (April 9, 2020): 577–81. http://dx.doi.org/10.4314/tjpr.v19i3.17.
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Purpose: To investigate the antiproliferative effect of the Red Sea cone snail, Conus geographus, against 4 MCF-7 (breast), MDA-MB-231 (epithelial human breast), HepG2 (hepatocellular) and SKOV-3 (ovarian) cancer cell lines.
Methods: Extraction of Red Sea cone snail sample with a mixture of CH2Cl2 and CH3OH (1:1, v/v) yielded 0.55 g of a green viscous material. The cytotoxic effects of the organic extract against the cancer cell lines were determined using cell proliferation (MTT) assay, and the half-maximal concentration (IC50) values measured. The effect of the crude extract on the cell cycle of the HepG-2 was determined by flow cytometry.
Results: The extract produced significant inhibitory effects against SKOV-3, MDA-MB-231, MCF-7 and HepG2, with IC50 values of 22.7 ± 2.2, 68.7 ± 6.2, 47 ± 4.2 and 19 ± 2.1 μg/mL, respectively. Cell cycle analysis revealed that the extract enhanced accumulation of HepG2 cells in the Go/G1 phase, at a level of 23.4 and 24.1 % at IC50 (19 μg/mL) and ½ IC50 (9.5 μg/mL), respectively, when compared to the untreated cells.
Conclusion: These results indicate that C. geographus extract exhibits potent cytotoxic effect against HepG2 cells via a mechanism involving G0/G1 cell cycle arrest. Thus, C. geographus is a potential source of a new anti-cancer agent.
Keywords: Conus geographus, Marine invertebrate, HepG2, Antiproliferation
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Lin, Xiaogang, Wenchao Li, Changbin Ye, Xiaozhu Liu, Hao Zhu, Wenbing Peng, and Jie Rong. "Research on the Interaction between Tubeimoside 1 and HepG2 Cells Using the Microscopic Imaging and Fluorescent Spectra Method." Computational and Mathematical Methods in Medicine 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/470452.
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The treatment of cancer draws interest from researchers worldwide. Of the different extracts from traditional Chinese medicines, Tubeimoside 1 (TBMS 1) is regarded as an effective treatment for cancer. To determine the mechanism of TBMS 1, the shape/pattern of HepG2 cells based on the microscopic imaging technology was determined to analyze experimental results; then the fluorescent spectra method was designed to investigate whether TBMS 1 affected HepG2 cells. A three-dimensional (3D) fluorescent spectra sweep was performed to determine the characteristic wave peak of HepG2 cells. A 2D fluorescent spectra method was then used to show the florescence change in HepG2 cells following treatment with TBMS 1. Finally, flow cytometry was employed to analyze the cell cycle of HepG2 cells. It was shown that TBMS 1 accelerated the death of HepG2 cells and had a strong dose- and time-dependent growth inhibitory effect on HepG2 cells, especially at the G2/M phase. These results indicate that the fluorescent spectra method is a promising substitute for flow cytometry as it is rapid and cost-effective in HepG2 cells.
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Tang, Zuxiong, Jun He, Jiayue Zou, Shufei Yu, Xiaoming Sun, and Lei Qin. "Cisplatin-resistant HepG2 cell-derived exosomes transfer cisplatin resistance to cisplatin-sensitive cells in HCC." PeerJ 9 (April 13, 2021): e11200. http://dx.doi.org/10.7717/peerj.11200.
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Backgrounds Cancer cell resistance to chemotherapy drugs such as Gemcitabine, Oxaliplatin, Cisplatin, Doxorubicin, and 5-fluorouracil account for the main reason of chemotherapy failure for HCC patients, especially for those with advanced HCC or metastasis patients. This emerging resistance limits the effectiveness and clinical application of these chemotherapy drugs. Previous studies reported that drug-resistant tumor cell-derived exosomes could transfer their resistance property to tumor sensitive cells in some cancer, including lung and gastric cancer. This study sought to explore whether HepG2/DDP cell-derived exosomes transmit cisplatin (DDP) resistance to HepG2 and other HCC sensitive cells, and provide considerable guidance for HCC nursing with Cisplatin DDP clinically. Methods The HepG2 DDP-resistant cell line (HepG2/DDP) was established, and the exosomes from both HepG2/DDP and HepG2 cells were isolated and named ES-2, ES-1, respectively. HepG2 or SMMC-7721 or Huh7 cells were treated with DDP or DDP + ES-2, and HepG2/DDP cells were treated with ES-1. Then, the activation of drug resistance via HepG2/DDP exosomes transfer to HepG2, SMMC-7721 and Huh7 cells were assessed by cell viability assay and ROS formation. Moreover, the relative expression of P-glycoprotein (P-gp) was measured by western blot analysis. Results HepG2/DDP cell-derived exosomes were successfully isolated from cisplatin-resistant HepG2 cells, and named ES-2. Cell viability of HepG2 or SMMC-7721 or Huh7 cells treated with DDP + ES-2 was enhanced compared with that of DDP treatment group. Also, the concentration of ROS generated in cells under DDP or DDP + ES-2 treatment was strongly increased compared with that of control, although the concentration of ROS was clearly smaller in DDP + ES-2 treatment group compared with DDP treatment. At the same time, the expression of P-gp was upregulated on the ES-2 surface. Conclusion The results mentioned above clarified that HepG2/DDP cell-derived exosomes conferred cisplatin resistance to HepG2 and other HCC cell lines, and provided a new significance for improving the effectiveness of DDP in treating HCC.
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Jiang, Guojun, Jiahua Hu, Junhe Huang, Yan Li, Qing Deng, Wenyan Jiang, Guihong Huang, and Qingqing Wang. "The Effect of Isoquercitrin on Cell Apoptosis and Cycle for HepG2 Cells." Scholars Academic Journal of Pharmacy 11, no. 10 (November 29, 2022): 182–86. http://dx.doi.org/10.36347/sajp.2022.v11i10.002.
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Purpose: To study the effect of isoquercitrin on cell apoptosis and cycle of HepG2 cells. Materials and Method: Different concentrations of isoquercitrin were used to act on HepG2 cells, and the effect of isoquercitrin on the proliferation of HepG2 cells was detected by CCK8. Cell morphology and growth were observed under inverted microscope. Flow cytometry was used to detect the apoptosis and cycle changes of HepG2 cells. Results: CCK8 found that isoquercitrin inhibited the growth of HepG2 cells, and it was correlated with the concentration and action time of isoquercitrin. Under the inverted microscope, it was observed that the number of cell survival gradually decreased with the increase of concentration or time of isoquercitrin acted on HepG2 cells. Flow cytometry showed that with the increase of isoquercitrin concentration, the number of cells blocked in S phase gradually decreased and the number of cells blocked in G2/M phase gradually increased. Conclusion: Isoquercitrin can induce apoptosis of HepG2 cells and interfere with S phase and G2/M phase in cell cycle.
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Turnbull, Patrick C., Ali C. Dehghani, Christopher F. Theriau, Michael K. Connor, and Christopher G. R. Perry. "Synergistic activation of mitochondrial metabolism and the glutathione redox couple protects HepG2 hepatocarcinoma cells from palmitoylcarnitine-induced stress." American Journal of Physiology-Cell Physiology 317, no. 6 (December 1, 2019): C1324—C1329. http://dx.doi.org/10.1152/ajpcell.00366.2019.
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Fatty acid stress can have divergent effects in various cancers. We explored how metabolic and redox flexibility in HepG2 hepatocarcinoma cells mediates protection from palmitoylcarnitine. HepG2 cells, along with HCT 116 and HT29 colorectal cancer cells were incubated with 100 μM palmitoylcarnitine for up to 48 h. Mitochondrial H2O2 emission, glutathione, and cell survival were assessed in HT29 and HepG2 cells. 100 μM palmitoylcarnitine promoted early growth in HepG2 cells by ~8% after 48 h versus decreased cell survival observed in HT29 and HCT 116 cells. Palmitoylcarnitine increased mitochondrial respiration at physiological and maximal concentrations of ADP, while lowering cellular lactate content in HepG2 cells, suggesting a switch to mitochondrial metabolism. HepG2 cell growth was associated with an early increase in H2O2 emission by 10 min, followed by a decrease in H2O2 at 24 h that corresponded with increased glutathione content, suggesting a redox-based compensatory mechanism. In contrast, abrogation of HT29 cell proliferation was related to decreased mitochondrial respiration (likely due to cell death) and decreased glutathione. Concurrent glutathione depletion with BSO prevented palmitoylcarnitine-induced growth in HepG2 cells, indicating that glutathione was critical for promoting growth following palmitoylcarnitine. Inhibiting UCP2 with genipin sensitized HepG2 cells to palmitoylcarnitine, suggesting that activation of UCP2 may be a 2nd redox-based mechanism conferring protection. These findings suggest that HepG2 cells possess inherent metabolic and redox flexibility relative to HT29 cells that confers protection from palmitoylcarnitine-induced stress via adaptive increases in mitochondrial respiratory control, glutathione buffering, and induction of UCP2.
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Dou, Chen-Zhuo, Yan-Fen Liu, Lu-Lu Zhang, Shao-Hong Chen, Chuan-Yin Hu, You Liu, and Yun-Tao Zhao. "Polyphenols from Broussonetia papyrifera Induce Apoptosis of HepG2 Cells via Inactivation of ERK and AKT Signaling Pathways." Evidence-Based Complementary and Alternative Medicine 2021 (March 23, 2021): 1–11. http://dx.doi.org/10.1155/2021/8841706.
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The extract of Broussonetia papyrifera has been proved to have antitumor activity. However, the underlying mechanism remains unclear. This study aimed to elucidate the mechanism of apoptosis of HepG2 cells induced by polyphenols from Broussonetia papyrifera (PBPs). The results revealed that PBPs inhibited the proliferation of HepG2 cells in a dose-dependent and time-dependent manner. Flow cytometry analysis showed that PBPs increased the apoptosis ratio of HepG2 cells significantly. PBPs increased intracellular reactive oxygen species (ROS) production and decreased intracellular superoxide dismutase (SOD) level of HepG2 cells. PBPs induced cell cycle arrest at G1 phase. Western blotting showed that PBPs upregulated the ratio of Bax/Bcl-2 and the expression level of Caspase-3, and activated p53 in HepG2 cells. The inhibition of proliferative relative signals (protein kinase B, PKB/AKT) and survival relative signals (extracellular signal-regulated kinase, ERK) were also observed in PBP-treated HepG2 cells. Our findings suggest that apoptosis of HepG2 cells induced by PBPs is mitochondria-mediated via inactivation of ERK and AKT signaling pathways.
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Bahgat, Mahmoud Mohamed, Mohamed Abd-Elhafez El-Far, Ahmed Atef Mesalam, Amany Abd-Elghany Ismaeil, Ahmed Atef Ibrahim, Hossam Eid Gewaid, Amany Sayed Maghraby, Mohamed Ahmed Ali, and Dina Nadeem Abd-Elshafy. "Schistosoma mansoni soluble egg antigens enhance HCV replication in mammalian cells." Journal of Infection in Developing Countries 4, no. 04 (February 25, 2010): 226–34. http://dx.doi.org/10.3855/jidc.522.
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Background: This work demonstrates successful propagation of HCV in HepG2 and human blood cells as well as viral shedding into their culture media. The influence of Schistosoma mansoni crude soluble egg antigens (SEA) on the rate of viral propagation in both mammalian cells was also monitored. Methodology: HepG2 cells were inoculated with HCV viremic human sera and some wells were exposed to HCV infection in presence of SEA. Cells were harvested for RT-PCR and Western blotting analysis. HepG2 media was collected for HCV ELISA. Blood samples from HCV-infected humans were cultured in the presence and absence of SEA. Media were collected at different time points post culturing and subjected to HCV ELISA. Results: The ELISA concentration of HCV antigens were generally higher in media of infected HepG2 cells compared to media of control cells at all time intervals post infection. Western blots showed reactivity to immunogenic peptides of different molecular weights in lysate of infected HepG2 cells that were not evidenced in uninfected cells. In presence of SEA, RT-PCR results revealed earlier detection of viral RNA in infected HepG2 cells compared to in absence of such bilharzial antigen. Also, ELISA results revealed higher levels of detected HCV antigens in media of both infected HepG2 and blood cells cocultured with S. mansoni SEA compared to that of cultured infected cells in absence of the parasite antigens. Conclusion: HepG2 cells as well as whole blood cultures maintain HCV replication. Furthermore, SEA has the potential to enhance HCV propagation.
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Pan, Jingbo, Zhaorui Lian, Sarah Wallet, and Mark A. Feitelson. "The hepatitis B x antigen effector, URG7, blocks tumour necrosis factor α-mediated apoptosis by activation of phosphoinositol 3-kinase and β-catenin." Journal of General Virology 88, no. 12 (December 1, 2007): 3275–85. http://dx.doi.org/10.1099/vir.0.83214-0.
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Hepatitis B x antigen (HBxAg) contributes significantly to the pathogenesis of chronic infection and development of hepatocellular carcinoma. To discern some of its operative pathways, HepG2 cells were stably transduced with HBx or the bacterial chloramphenicol acetyltransferase (CAT) gene. Differential gene expression has previously revealed an upregulated gene, clone 7 (URG7), that conferred resistance to anti-Fas killing on HepG2X cells. Given that tumour necrosis factor alpha (TNFα) is also an important mediator of chronic hepatitis, and partially shares signalling with Fas, experiments were designed to test whether URG7 blocks TNFα killing of HepG2X cells. HepG2X cells expressing URG7 and HepG2 cells overexpressing URG7 in the absence of HBxAg were resistant to TNFα killing compared with HepG2CAT cells. URG7 small interfering RNA restored the sensitivity of HepG2X cells to TNFα killing. Killing was associated with the activation of caspases 3 and 8, suggesting that URG7 blocked these caspases. This resistance was also associated with activation of phosphoinositol 3-kinase/Akt. Given that Akt and HBxAg also activate β-catenin, experiments were designed to determine whether URG7 blocked apoptosis via activation of β-catenin. Both HBxAg and URG7 activated fragments of the β-catenin promoter, and also promoted expression of β-catenin target genes. Hence, URG7 inhibits TNFα-mediated killing by blocking one or more caspases in the apoptotic pathway and by activating phosphoinositol 3-kinase and β-catenin, thereby overriding the apoptotic signalling of TNFα. This suggests that URG7 helps to protect virus-infected hepatocytes during chronic hepatitis B virus infection.
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Izdebska, Magdalena, Mariola Herbet, Monika Gawrońska-Grzywacz, Iwona Piątkowska-Chmiel, Agnieszka Korga, Marcin Sysa, Magdalena Iwan, et al. "Resveratrol Limits Lipogenesis and Enhance Mitochondrial Activity in HepG2 Cells." Journal of Pharmacy & Pharmaceutical Sciences 21 (December 7, 2018): 504–15. http://dx.doi.org/10.18433/jpps29994.
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Purpose: The aim of this study was to evaluate the effect of resveratrol on de novo lipogenesis in HepG2 cells caused by high glucose concentrations. Increased lipogenesis in the liver is the main reason for the development of nonalcoholic fatty liver disease (NAFLD) - currently one of the most common chronic liver diseases. In developed countries, this disease is mostly associated with nutritional disorders, resulting from the increasing consumption of monosaccharides. Resveratrol is a natural polyphenol with a promising potential for NAFLD treatment. Methods: The steatosis of HepG2 cells was visualized using the intracellular lipid staining by Nile Red dye with a fluorescence microscope. This study also evaluated the effect of resveratrol on the mitochondrial activity (MitoTracker Green staining), dsDNA (Hoechst 33342 staining) and the viability of HepG2 cells treated with high glucose concentrations (25 and 33 mM). Results: Current study showed that high glucose concentrations induced fat-overloading in HepG2 cells (microvacuolar steatosis occurred in most of the cells). Resveratrol (20 μM) limits the steatosis induction in HepG2 cells by glucose and increased the mitochondrial activity of cells. Resveratrol did not affect the viability of HepG2 cells. Conclusion: This beneficial effect could be helpful in the treatment of NAFLD.
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Kiseleva, Y. Y., K. G. Ptitsyn, O. V. Tikhonova, S. P. Radko, LK Kurbatov, I. V. Vakhrushev, V. G. Zgoda, E. A. Ponomarenko, A. V. Lisitsa, and A. I. Archakov. "PCR analysis of the absolute number of copies of human chromosome 18 transcripts in liver and HepG2 cells." Biomeditsinskaya Khimiya 63, no. 2 (2017): 147–53. http://dx.doi.org/10.18097/pbmc20176302147.
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Using reverse transcription in conjunction with the quantitative real-time PCR or digital droplet PCR, the transcriptome profiling of human chromosome 18 has been carried out in liver hepatocytes and hepatoblastoma cells (HepG2 cell line) in terms of the absolute number of each transcript per cell. The transcript abundance varies within the range of 0.006 to 9635 and 0.011 to 4819 copies per cell for HepG2 cell line and hepatocytes, respectively. The expression profiles for genes of chromosome 18 in hepatocytes and HepG2 cells were found to significantly correlate: the Spearman's correlation coefficient was equal to 0.81. The distribution of frequency of transcripts over their abundance was bimodal for HepG2 cells and unimodal for liver hepatocytes. Bioinformatic analysis of the differential gene expression has revealed that genes of chromosome 18, overexpressed in HepG2 cells compared to hepatocytes, are associated with cell division and cell adhesion processes. It is assumed that the enhanced expression of those genes in HepG2 cells is related to the proliferation activity of cultured cells. The differences in transcriptome profiles have to be taken into account when modelling liver hepatocytes with cultured HepG2 cells.
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Lin, Kwang-huei, Hsing-ying Shieh, and Hai-Chu Hsu. "Negative Regulation of the Antimetastatic Gene Nm23-H1 by Thyroid Hormone Receptors*." Endocrinology 141, no. 7 (July 1, 2000): 2540–47. http://dx.doi.org/10.1210/endo.141.7.7570.
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Metastasis of various malignant cells is inversely related to the abundance of the Nm23-H1 protein. The possible role of thyroid hormones in tumor metastasis has now been investigated by examining the effect of T3 on the expression of the Nm23-H1 gene. Human hepatoma HepG2 cells, in which endogenous thyroid hormone receptor subtype α1 (TRα1) is expressed at a low level, were stably transfected, either with expression plasmids encoding wild-type TRα1 or a dominant negative mutant of TRα1, or with the empty vector (yielding HepG2-Wt, HepG2-Mt, and HepG2-Neo cells, respectively). Immunoblot analysis revealed that exposure of HepG2-Wt and HepG2-Neo cells, but not HepG2-Mt cells, to T3-induced time-dependent decreases in the abundance of Nm23-H1 messenger RNA and protein, with the extent of these effects correlating with the level of expression of TRα1. An in vitro assay also revealed that T3 induced a marked increase in the invasive activity of HepG2-Wt cells; it induced a smaller increase in that of HepG2-Neo cells but had no effect on that of HepG2-Mt cells. Finally, the promoter region of Nm23-H1 spanning nucleotides −471 to− 437 (relative to the transcriptional initiation site) inhibited the expression of a downstream reporter gene, in a T3-dependent manner, in COS-1 cells also transfected with an expression plasmid encoding TRα1 or TRβ1. The DNA binding domain of TRβ1 was required for this inhibitory effect. These results indicate that T3, acting through TRs, inhibits transcription of Nm23-H1, and that this effect is mediated by a negative regulatory element in the promoter region of the gene. Thus, it is possible that T3 promotes tumor metastasis by inducing down-regulation of Nm23-H1 expression.
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Singh, Pankaj Kumar, Raj Kumar, Ashok Sharma, Rajesh Arora, Raman Chawla, Swatantra Kumar Jain, Rajendra Prasad Tripathi, and Rakesh Kumar Sharma. "Role of Apoptotic Proteins in REC-2006 Mediated Radiation Protection in Hepatoma Cell Lines." Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–11. http://dx.doi.org/10.1093/ecam/neq059.
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The present study was carried out to evaluate the role of apoptotic proteins in REC-2006-mediated radiation protection in hepatoma cell lines. REC-2006 treatment 2 h before irradiation strongly inhibited the cleavage of ATM and PARP-1 in HepG2 cells. The expression of nuclear apoptosis inducing factor (AIF) was found to be more inhibited (~17%) in HepG2 cells in REC-2006 + radiation-treated group. More inhibition (~33%) of cytochromecwas observed in HepG2 cells upon REC-2006 treatment 2 h prior irradiation. Similarly, significantly more (P<.05) inhibition of Apaf-1, caspase-9 and caspase-3 was observed in REC-2006 + radition-treated group in HepG2 cells. REC-2006 treatment restored the expression of ICAD in HepG2 cells; however, no restoration was observed in Hep3B cells. Lower nuclear to cytoplasmic CAD ratio was observed in HepG2 cells (~0.6) as compared with Hep3B cells (~1.2) in REC-2006 + radiation-treated group. In conclusion, REC-2006 rendered higher protection in HepG2 cells by inhibiting the expression and translocation of AIF, inhibiting the cleavage of ATM and PARP-1, restoring the expression of ICAD, inhibiting the release of cytochromecand thus modulating the expression of Apaf-1 caspase-9 and activity of caspase-3.
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Okita, Yamato, Takeru Shiono, Ayano Yahagi, Satoru Hamada, Masayuki Umemura, and Goro Matsuzaki. "Interleukin-22-Induced Antimicrobial Phospholipase A2 Group IIA Mediates Protective Innate Immunity of Nonhematopoietic Cells against Listeria monocytogenes." Infection and Immunity 84, no. 2 (December 7, 2015): 573–79. http://dx.doi.org/10.1128/iai.01000-15.
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Listeria monocytogenesis a bacterial pathogen which establishes intracellular parasitism in various cells, including macrophages and nonhematopoietic cells, such as hepatocytes. It has been reported that several proinflammatory cytokines have pivotal roles in innate protection againstL. monocytogenesinfection. We found that a proinflammatory cytokine, interleukin 22 (IL-22), was expressed by CD3+CD4+T cells at an early stage ofL. monocytogenesinfection in mice. To assess the influence of IL-22 onL. monocytogenesinfection in hepatocytes, cells of a human hepatocellular carcinoma line, HepG2, were treated with IL-22 beforeL. monocytogenesinfectionin vitro. Gene expression analysis of the IL-22-treated HepG2 cells identified phospholipase A2 group IIA (PLA2G2A) as an upregulated antimicrobial molecule. Addition of recombinant PLA2G2A to the HepG2 culture significantly suppressedL. monocytogenesinfection. Culture supernatant of the IL-22-treated HepG2 cells contained bactericidal activity againstL. monocytogenes, and the activity was abrogated by a specific PLA2G2A inhibitor, demonstrating that HepG2 cells secreted PLA2G2A, which killed extracellularL. monocytogenes. Furthermore, colocalization of PLA2G2A andL. monocytogeneswas detected in the IL-22-treated infected HepG2 cells, which suggests involvement of PLA2G2A in the mechanism of intracellular killing ofL. monocytogenesby HepG2 cells. These results suggest that IL-22 induced at an early stage ofL. monocytogenesinfection enhances innate immunity againstL. monocytogenesin the liver by stimulating hepatocytes to produce an antimicrobial molecule, PLA2G2A.
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Zhang, H., L. W. Zhang, and W. C. Liu. "Specific immune responses against hepatocellular carcinoma induced by dendritic cell- HepG2 fusion cells derived- exosomes." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 13511. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.13511.
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13511 Background: To assess the properties of exosomes secreted by fusion cells of hepatoma patient-derived dendritic cells(DCs)and hepatoma cell line (HepG2) and to evaluate the function of these exosomes to trigger efficient T cell responses against HepG2 cells in vitro. Methods: Peripheral blood mononuclear cells (PBMC) from hepatoma patients were isolated and in the presence of GM-CSF and IL-4, PBMC were cultured in vitro for one week to induce dendritic cells (DC). Fusion cells of DC with HepG2 cells (DC- HepG2) were achieved by PEG and were isolated by magnetic device with HLA Class II Dynabeads. Exosomes were then prepared from the supernatants of the fusion cells by ultra filtration centrifugation and sucrose gradient ultracentrifugation. T lymphocytes were pulsed with exosomes directly in the presence of IL-2. After co-cultured with target cells, the stimulated lymphocytes were tested by IFN-? release assay and cytotoxicity capacity assay. Results: After fusion, DC-HepG2 expressed expressed high level of DC surface molecules, including CD83 87.4%, CD80 94.9%, CD86 90.13% and HLA-DR 98.62%. Application of the isolation procedure to fusion cells also revealed exosome vesicles by transmission electron microscopy. Protein analysis by FCM was performed and revealed that the costimulatory molecule CD86 and AFP protein was detectable. The fusion cell- derived exosomes could directly activate T lymphocytes which lysed HepG2 target cells much more effectively than T cells alone did (P<0.05). To determine whether the lysis was HepG2 tumor cell-specific, SMMC7721 and K562 cells were used as target cells and nearly no lysis of these cells was observed. Furthermore, IFN-? in the culture supernatants of exosomes- activated T cells was significantly higher than that in normal control T cells (P<0.05). Conclusions: Exosomes could be purified from the supernatants of fusion cells. These exosomes could activate T cells directly and could induce effective HepG2 secific CTL responses. DC- HepG2 fusion cells-derived exosomes may represent as a promising approach of immunotherapy for HCC. No significant financial relationships to disclose.
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Nguyen, Sinh Truong, Phuc Hong Vo, Oanh Thi-Kieu Nguyen, Nghia Minh Do, and Phuc Van Pham. "ID: 1085 Sodium citrate induces apoptosis in HepG2 cell lines." Biomedical Research and Therapy 4, S (September 5, 2017): 174. http://dx.doi.org/10.15419/bmrat.v4is.359.
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PURPOSES: Cancer cells were observed to increase glucose uptake and fermentation of glucose to lactate to to synthesis rapidly ATP for cell growth, survival and proliferation. Thus, inhibition of glycolysis might be useful in antitumor treatment. This phenomenon occurred even with fully functioning mitochondria, and known as Warberg effect. Sodium citrate, an inhibitor of Warberg effect, was reported to antiproliferate many cancer cells line. However, sodium citrate has not been studied in Hepatocellular Carcinoma cells line yet. Here we aimed to investigate the effect of sodium citrate in HepG2 cells line.
MATERIAL AND METHODS: HepG2 cell lines was treated with sodium citrate at different concentrations. Viable cells were determined by Alamar Blue. The apoptosis induced-cells was detected by Annexin V with FCM technique. Disintegrated nuclei and DNA fragmentation was analyzed. The activity of caspase-3 was also tested.
RESULTS: We observed that the IC50 value of sodium citrate on HepG2 is at 10mM. FCM analysis showed that sodium citrate induced apoptosis in HepG2 cell line in dose-dependent manner. At 10mM sodium citrate, the caspase-3/7 was observed to be activated in time-dependent manner. Sodium citrate also induced nuclei disintergated in HepG2. DNA fragmentation was observed when HepG2 cells were treated with 10mM sodium citrate.
CONCLUSIONS: We have shown that sodium citrate possesses the antiproliferative ability on HepG2 at IC50 10mM. Sodidum citrate induces apoptosis cells in hepatocellular carcinoma HepG2 by capases-3 activation. More investigation of glycolysis inhibition of sodium citrate on HepG2 should be performed in animals
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Yusuf, Hanifah, Marhami Fahriani, and Cut Murzalina. "ANTICANCER ACTIVITY OF ETHANOL EXTRACT OF YELLOW ROOT (Arcangelisia flava) ON HEPG2 HEPATOCELLULAR CANCER CELLS." Jurnal Kedokteran Hewan - Indonesian Journal of Veterinary Sciences 16, no. 1 (April 14, 2022): 18–22. http://dx.doi.org/10.21157/j.ked.hewan.v16i1.23615.
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This study aimed to evaluate anticancer activity and apoptosis induction of ethanolic extract of Arcalengisia flava (AF) roots on HepG2 cancer cell lines. The AF roots were extracted by maceration using ethanol 80%. MTT assay method was used to evaluate the anticancer activity and the proliferation of HepG2 cells. Flow cytometry method was used to assess the induction of HepG2 cells apoptosis. This study showed that the IC50 of AF ethanol extract against HepG2 cells was 109.14 μg/ml. With IC50 treatment, the apoptosis assay showed a significant decrease in intact cells (80.10±1.7%) and a significant increase in early apoptosis (7.9±0.7%) and late apoptosis cells of HepG2 cancer cells (4.9±0.35%) compared to control cells. Moreover, the proliferation of HepG2 cells was declined significantly in 48 and 72 hours after treatment with IC50 (77.5±5.76% and 64.3±5.37%, respectively) and 2xIC50 of the extract (75.9±1.79% and 70.5±4.27%, respectively). This research suggests that the ethanolic extract of AF roots can potentially be used for hepatocarcinoma treatment.
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Hu, Die, Shintaro Fumoto, Hirotaka Miyamoto, Masakazu Tanaka, and Koyo Nishida. "Flavonoids Enhance Lipofection Efficiency and Ameliorate Cytotoxicity in Colon26 and HepG2 Cells via Oxidative Stress Regulation." Pharmaceutics 14, no. 6 (June 5, 2022): 1203. http://dx.doi.org/10.3390/pharmaceutics14061203.
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The generation of reactive oxygen species (ROS) can affect cationic liposome-mediated transfection. In this study, we focused on a specific class of antioxidants, flavonoids, to investigate the transfection efficiency using cationic liposome/plasmid DNA complexes (lipoplexes) in 2D and 3D cultures of Colon26 and HepG2 cells, respectively. All tested flavonoids enhanced the transfection efficiency in 2D Colon26 and HepG2 cells. Among the tested flavonoids, 25 µM quercetin showed the highest promotion effect of 8.4- and 7.6-folds in 2D Colon26 and HepG2 cells, respectively. Transfection was also performed in 3D cultures of Colon26 and HepG2 cells using lipoplexes with quercetin. Quercetin (12.5 µM) showed the highest transfection efficiency at all transfection timings in 3D Colon26 and HepG2 cells with increased cell viability. Flow cytometry revealed that quercetin treatment reduced the population of gene expression-negative cells with high ROS levels and increased the number of gene expression-positive cells with low ROS levels in HepG2 cells. Information from this study can be valuable to develop strategies to promote transfection efficiency and attenuate cytotoxicity using lipoplexes.
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Kawase, Atsushi, Ouka Takashima, Satsuki Tanaka, Hiroaki Shimada, and Masahiro Iwaki. "Diclofenac-Induced Cytotoxicity in Direct and Indirect Co-Culture of HepG2 Cells with Differentiated THP-1 Cells." International Journal of Molecular Sciences 23, no. 15 (August 4, 2022): 8660. http://dx.doi.org/10.3390/ijms23158660.
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Non-steroidal anti-inflammatory drugs (NSAIDs) such as diclofenac (DIC) frequently induce drug-induced liver injury (DILI). It is unclear whether macrophages such as M1 and M2 participate in NSAID-associated DILI; elucidating this relationship could lead to a better understanding of the detailed mechanism of DILI. We co-cultured human hepatoma HepG2 cells with M1 or M2 derived from human monocytic leukemia THP-1 cells to examine the roles of M1 and M2 in DIC-induced cytotoxicity. DIC was added to the direct or indirect co-cultures of HepG2 cells with M1 or M2 (HepG2/M1 or HepG2/M2, respectively) at cell ratios of (1:0, 1:0.1, 1:0.4, and 1:1). In both direct and indirect HepG2/M2 co-cultures (1:0.4), there was lower lactate dehydrogenase release compared with HepG2/M1 co-cultures. Other NSAIDs as well as DIC showed similar protective effects of DIC-induced cytotoxicity. There were only slight differences in mRNA levels of apoptosis- and endoplasmic reticulum stress-associated factors between M1 and M2 after DIC treatment, suggesting that other factors determined the protective effects of M2 on DIC-induced cytotoxicity. Levels of high mobility group box 1 (HMGB1) in the medium and the mRNA expression levels of HMGB1 receptors were different between M1 and M2 after DIC treatment. Increased HMGB1 concentrations and expression of toll-like receptor 2 mRNA in M1 were observed compared with M2 after DIC treatment. In conclusion, these results suggested that the HMGB1/TLR2 signaling axis can be suppressed in M2 but not M1, leading to the different roles of M1 and M2 in NSAID-induced cytotoxicity.
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Hiramatsu, N., S. Dash, and M. A. Gerber. "HCV cDNA transfection to HepG2 cells." Journal of Viral Hepatitis 4, s1 (September 1997): 61–67. http://dx.doi.org/10.1111/j.1365-2893.1997.tb00162.x.
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Yu, Lei, Xin Wang, Zhi-Feng Chen, Bo Jiang, Dong-Yu Shang, Yong-Xue Sun, Jing-Hui Yang, Lian-Fang Zhang, and Yu-Bin Ji. "Cytisine induces apoptosis of HepG2 cells." Molecular Medicine Reports 16, no. 3 (March 2017): 3363–70. http://dx.doi.org/10.3892/mmr.2017.6991.
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Maurici, D., V. Campi, I. Malerba, M. Carfi, G. Bowe, and L. Gribaldo. "458 Styrene toxicity in HEPG2 cells." Toxicology Letters 144 (September 2003): s123. http://dx.doi.org/10.1016/s0378-4274(03)90457-7.
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Huang, Rongrong, Zhongsi Chen, Mei Liu, Yan Deng, Song Li, and Nongyue He. "The aptamers generated from HepG2 cells." Science China Chemistry 60, no. 6 (April 5, 2017): 786–92. http://dx.doi.org/10.1007/s11426-016-0491-7.
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Chen, Yaxi, Xiong Z. Ruan, Qiu Li, Ailong Huang, John F. Moorhead, Stephen H. Powis, and Zac Varghese. "Inflammatory cytokines disrupt LDL-receptor feedback regulation and cause statin resistance: a comparative study in human hepatic cells and mesangial cells." American Journal of Physiology-Renal Physiology 293, no. 3 (September 2007): F680—F687. http://dx.doi.org/10.1152/ajprenal.00209.2007.
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LDL receptor (LDLr) is widely expressed in both liver and peripheral tissue. We aimed to clarify tissue-specific regulation of LDLr in hepatic cell line (HepG2) cells and human kidney mesangial cells (HMCs) under physiological and inflammatory conditions. We have demonstrated that the concentration of LDL required for 50% inhibition of LDLr mRNA expression (IC50) in HepG2 was 75 μg/ml, but only 30 μg/ml in HMCs. The concentration of mevastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, which achieved 200% upregulation of LDLr (UC200) in HepG2 cells, was 0.7 μM, which is much lower than 2.8 μM in HMCs. Inflammatory stress increased IC50 to 80 and 75 μg/ml of LDL, UC200 to 2.8 μM, and 4.2 μM of mevastatin in HepG2 and HMCs. There was obvious sterol-regulatory element binding protein cleavage-activating protein accumulation in the Golgi in HepG2 cells, but not in HMCs in the presence of high concentration of LDL. IL-1β further increased sterol-regulatory element binding protein cleavage-activating protein accumulation in HepG2 and HMCs in the presence of high concentration of LDL. These results indicate that LDLr in HepG2 cells have a relative resistant phenotype for downregulation, while LDLr in HMCs is very sensitive for downregulation. Inflammatory cytokine disrupts LDLr negative feedback regulation induced by intracellular cholesterol in both cell types, to a greater degree in HMCs, which could be one reason why HMCs are more prone to become foam cells under inflammatory stress. Inflammation also causes statin resistance; therefore, a high concentration of statin may be required to achieve the same biological effect.
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Kim, Moon, Deok Sim, Hye Lee, Hyo-Jung Lee, and Sung-Hoon Kim. "Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC." International Journal of Molecular Sciences 20, no. 3 (January 29, 2019): 582. http://dx.doi.org/10.3390/ijms20030582.
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Although shikimic acid from Illicium verum has antioxidant, antibacterial, anti-inflammatory, and analgesic effects, the effect of shikimic acid on lipogenesis has not yet been explored. Thus, in the present study, hypolipogenic mechanism of shikimic acid was examined in HepG2, Huh7 and 3T3-L1 adipocyte cells. Shikimic acid showed weak cytotoxicity in HepG2, Huh7 and 3T3-L1 cells, but suppressed lipid accumulation in HepG2, Huh7 and 3T3-L1 cells by Oil Red O staining. Also, shikimic acid attenuated the mRNA expression of de novo lipogenesis related genes such as FAS, SREBP-1c, and LXR-α in HepG2 cells by RT-PCR analysis and suppressed the protein expression of SREBP-1c and LXR-α in HepG2 and 3T3-L1 cells. It should be noted that shikimic acid activated phosphorylation of AMP-activated protein kinase (AMPK)/Aacetyl-coenzyme A carboxylase (ACC) and reduced the expression of MID1 Interacting Protein 1 (MID1IP1) in HepG2, Huh7 and 3T3-L1 cells. Conversely, depletion of MID1IP1 activated phosphorylation of AMPK, while overexpression of MID1IP1 suppressed phosphorylation of AMPK in HepG2 cells. However, AMPK inhibitor compound c did not affect the expression of MID1IP1, indicating MID1IP1 as an upstream of AMPK. Taken together, our findings suggest that shikimic acid has hypolipogenic effect in HepG2 and 3T3-L1 cells via phosphorylation of AMPK/ACC and inhibition of MID1IP1 as a potent candidate for prevention or treatment of fatty liver and hyperlipidemia.
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Yingkun, Nie, Zhu Lvsong, and Yu Huimin. "Shikonin inhibits the proliferation and induces the apoptosis of human HepG2 cells." Canadian Journal of Physiology and Pharmacology 88, no. 12 (December 2010): 1138–46. http://dx.doi.org/10.1139/y10-085.
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This study investigated the potential of shikonin as an anticancer agent against liver cancer and an in vitro human hepatoma cancer model system. The HepG2 cell line was the hepatoma cancer model in the present study. The inhibitory effect of shikonin on the growth of HepG2 cells was measured by MTT assay. To explore the underlying mechanism of cell growth inhibition of shikonin, the cell cycle distribution, DNA fragmentation, mitochondrial membrane potential (Δ[Formula: see text]m) disruption, and expression of Bax and Bcl-2 were measured in HepG2 cells. The activity of shikonin in inducing apoptosis was investigated through the detection of Annexin V signal and CD95 expression by flow cytometry and electron microscopy, respectively. Shikonin inhibited the growth of HepG2 cells in a dose-dependent manner. The IC50 value (inhibiting cell growth by 50%) was 4.30 µg/mL. Shikonin inhibited cell growth in a dose-dependent manner and blocked HepG2 cell cycle progression at the S phase. The changes in mitochondrial morphology, dose-dependently decreased in Δ[Formula: see text]m, were observed in different concentrations of the drug treatment group. Western blot analysis showed that cajanol inhibited Bcl-2 expression and induced Bax expression. Furthermore, we show that shikonin increases Annexin V signal and CD95 (Fas/APO) expression, resulting in apoptotic cell death of HepG2 cells. In addition, lump formation of intranuclear chromatin, pyknosis of cell nucleus, deletion of microvillus, vacuolar degeneration of mitochondria, reduction of rough endoplasmic reticulum, and resolution of free ribosome, etc., associated with apoptosis were discovered by electron microscopy in HepG2 cells after 48 h treatment. Shikonin inhibited HepG2 cells, possibly through the pathway of inducing early apoptosis, and was beneficial for restoring the apoptotic sensitivity of HepG2 cells by CD95, and should therefore be considered as a candidate agent for the prevention or treatment of human hepatoma.
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Yurdakok, Begum, Emine Baydan, Hamza Okur, and Ismayil Safa Gurcan. "Cytotoxic effects of etephon and maleic hydrazide in Vero, Hep2, HepG2 cells." Drug and Chemical Toxicology 37, no. 4 (February 4, 2014): 459–65. http://dx.doi.org/10.3109/01480545.2014.884112.
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He, Ao-Di, Ming-Lu Liang, Gang Liu, Xing-Wen Da, Guang-Qiang Yao, Wen Xie, Ji-Zhou Xiang, Cunji Gao, and Zhang-Yin Ming. "The Role of FcγRIIa and TGF-β1/KLF6 Pathway in Platelet's Promoting Hepatocellular Carcinoma Cells Growth." Blood 124, no. 21 (December 6, 2014): 1429. http://dx.doi.org/10.1182/blood.v124.21.1429.1429.
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Abstract Background: Platelet in the primary tumor microenvironment plays a crucial role in tumor cells angiogenesis, growth, and metastasis. Clinical and experimental evidences support that platelets and their extracts influence hepatocellular carcinoma (HCC) growth and biology. But the mechanism is still not fully clarified. The aim of present study was to elucidate an unperceived mechanism of the proliferative effect of platelet on HCC cells. Methods: Human blood was collected from health volunteers, washed platelets were prepared and resuspended by fresh medium. The ability of HepG2 cells to induce platelet aggregation was analyzed using a Chrono-Log Lumi-aggregometer. HepG2 cells were incubated with platelets activated by thrombin (0.08 U/ml) and collagen-related peptide (CRP, 0.8μg/ml), or releasates isolated from CRP-stimulated platelets. The effect of platelet releasate on HepG2 cell proliferation was determined with the colorimetric 3-(4, 5-dimethylthiazol)-2, 5-diphenyltetrazolium bromide (MTT) assay. Western blot was used to measure expression of Krüppel-like factor 6 (KLF6) in HepG2 cells. Anti-FcγRIIa monoclonal antibody IV.3 (10μg/ml) and transforming growth factor beta 1 (TGF-β1) receptor inhibitor SB431542 (10μM) were used. Furthermore, KLF6 gene silence was also conducted in HepG2 cells by transfected with KLF6 siRNA. Results: Our data showed HepG2 cells (1.0×105/ml) could induce human washed platelet (3.0×108/ml) aggregation in vitro, indicating that HepG2 cells could activate platelets. We further verified that releasate from CRP-activated platelets could promote the proliferation of HepG2 cells. Importantly, this effect exhibits on the down expression of KLF6 in HepG2 cells. In presence and absence of platelet stimulator thrombin (0.08 U/ml) or collagen-related peptide (CRP, 0.8μg/ml), washed platelets could reduce KLF6 expression in HepG2 cells after incubated for 12 and 24 hours. Meanwhile, supernatant from CRP-activated platelets exhibited the same effect. On the other hand, the resuspended CRP-activated platelet pellet showed no significant influence on KLF6 expression. And platelets incubated with anti- FcγRIIa monoclonal antibody IV.3 (10μg/ml) and transforming growth factor beta 1 (TGF-β1) receptor inhibitor SB431542 (10μM) abolished the effects. Furthermore, the platelet’s promoting proliferation effect was attenuated in HepG2 cells with silencing KLF6 expression. Conclusion: Tumor cells could activate platelet, and activated platelet could regulate cancer cell progression in turn. We further verified that platelet, a main source of bioavailable TGF-β1, has a promoting effect on the proliferation of HepG2 cells. Importantly, this effect exhibits on the down expression of KLF6 in HepG2 cells, in which FcγRIIa and TGF-β1 involved. These results extend our understanding of mechanisms by which platelets contribute to tumor progression, which may provide a new therapeutic target for the prevention and treatment of HCC. Disclosures No relevant conflicts of interest to declare.
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Ji, Yu Bin, Fang Dong, Shi Yong Gao, and Miao Yu. "Study on Capparis spionosa L. Polysaccharide (CSPS) Induced HepG2 Apoptosis by Controlling Ca2+ Path." Advanced Materials Research 282-283 (July 2011): 203–8. http://dx.doi.org/10.4028/www.scientific.net/amr.282-283.203.
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To investigate the mechanism on Capparis spionosa L polysaccharide(CSPS) inducing apoptosis in HepG2 human hepatoma cell. MTT was ddopted to determine if CSPS had cytotoxic effect on HepG2. Morphology of HepG2 changed with dosages of CSPS was detected by laser confocal scanning microscope. Flow cytometry(FCM) was used to detect the apoptosis by PI labeling method. Calcium, mitochondrial membrane potential, Bcl-2/Bax of HepG2 cells were detected by laser confocal scanning microscope. The result of MTT showed that CSPS could inhibit the growth of HepG2 significantly. HepG2 cells were shrinkage, fragmentation, appearance of apoptotic bodies by laser confocal scanning microscope. HepG2 cell apoptosis rate was increased gradually with dosage by FCM. Calcium concentration, mitochondrial membrane potential, Bcl-2 protein of HepG2 were decreased, Bax protein content of HepG2 was increased by laser confocal scanning microscope. CSPS induced HepG2 apoptosis by controlling Bax/Bcl-2 in Ca2+ path.
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Cheng, Ke, Zhizhao Chen, Lian Liu, Yujun Zhao, Sheng Zhang, Qiang Wang, Zhenghao Deng, Sipin Tan, and Qifa Ye. "ZNF667 Serves as a Putative Oncogene in Human Hepatocellular Carcinoma." Cellular Physiology and Biochemistry 41, no. 6 (2017): 2523–33. http://dx.doi.org/10.1159/000475971.
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Background/Aims: Zinc finger protein 667 (ZNF667) is a member of C2H2 zinc finger protein family. For the first time, we aim to analyze the expression pattern of ZNF667 in hepatocellular carcinoma (HCC) tissues; to explore its role in HCC tumorigenesis. Methods: Immuno-histochemistry was carried out to characterize the ZNF667 expression in paraffin-embedded HCC samples. The relationship between ZNF667 expression and the clinical, pathological data of the patients were analyzed. Human normal hepatocyte cells LO2 over expressing ZNF667 (LO2-ZNF667 cells), ZNF667 depleted hepatocellular carcinoma HepG2 cells (HepG2-shZNF667 cells) were set up, their proliferation, migration and invasion abilities were analyzed. Xenograft nude mice were used to analyze the malignancy of HepG2-shZNF667 cells in vivo. Western blot was performed to analyze the expression of Bcl-2 and BAX in LO2-ZNF667 and HepG2-shZNF667 cells. Results: Increased ZNF667 was found via immuno-histochemistry in HCC. Enhanced ZNF667 expression was associated with tumor size, clinical stage and tumor differentiation. LO2-ZNF667 cells displayed increased and HepG2-shZNF667 cells decreased cell proliferation, migration and invasion. Xenograft experiments proved reduced malignancy of HepG2-shZNF667 cells in vivo. LO2-ZNF667 cells displayed increased Bcl-2 and decreased BAX protein expression. HepG2-shZNF667 cells displayed enhanced BAX and inhibited BCL-2 expression. Conclusions: ZNF667 is shown to be a new oncogene in HCC and it may serve as a new therapeutic target for HCC via enhancing BCL-2 and decreasing BAX expression.
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Wu, Lii-Tzu, Jing-Gung Chung, Jung-Chou Chen, and Wei Tsauer. "Effect of Norcantharidin on N-acetyltransferase Activity in HepG2 Cells." American Journal of Chinese Medicine 29, no. 01 (January 2001): 161–72. http://dx.doi.org/10.1142/s0192415x01000186.
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The inhibition of arylamine N-acetyltransferase (NAT) activity by norcantharidin (NCTD), the demethylated form of cantharidin, in human hepatocellular carcinoma HepG2 cells was investigated. By using high performance liquid chromatography, NAT activity on acetylation of 2-aminofluorene (AF) and p-aminobenzoic acid (PABA) were examined. Two assay system were performed, one with cellular cytosols, the other with intact HepG2 cell suspensions. The NAT activity in HepG2 cell line was inhibited by norcantharidin in a dose-dependent manner in both types of examined systems: i.e. the greater the concentration of norcantharidin in the reaction, the greater the inhibition of NAT activities. This report is the first to show that norcantharidin has an inhibitory effect on NAT activity in HepG2 cell.
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Sriset, Yollada, Waranya Chatuphonprasert, and Kanokwan Jarukamjorn. "Optimized models of xenobiotic-induced oxidative stress in HepG2 cells." Tropical Journal of Pharmaceutical Research 18, no. 5 (May 25, 2021): 1001–7. http://dx.doi.org/10.4314/tjpr.v18i5.13.
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Purpose: To evaluate the molecular impact of ethanol, sodium selenite, and tert-butyl hydroperoxide (TBHP) on oxidant-antioxidant balance in HepG2 cells to establish an optimized oxidative stress model of HepG2 cells.
Methods: HepG2 cells were treated with ethanol (10 - 500 mM) and sodium selenite (1 - 10 µM) for 24 and 48 h and with TBHP (50 - 200 µM) for 3 and 24 h, respectively. Biomarkers for cellular injury, ie, lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA), and for antioxidant system, i.e., superoxide dismutase (SOD), catalase (CAT), and total glutathione content, were determined.
Results: All treatments increased the levels of LDH, AST, ALT, and MDA but decreased SOD and CAT activities and the total glutathione content in HepG2 cells. Oxidative stress was induced by these oxidative stressors in HepG2 cells via oxidant-antioxidant imbalance, with TBHP (100 µM, 3 h) acting as a powerful oxidant based on the minimal time to induce oxidative stress. The antioxidants, ascorbic acid and gallic acid, improved oxidant-antioxidant imbalance against xenobiotic-induced oxidative stress in HepG2 cells.
Conclusion: These oxidative stress models are suitable for investigating the antioxidant and/or hepatoprotective potential of chemicals, including natural compounds.
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Zheng, Sheng, Hua Yang, Yefei Chang, Dan Zhao, and Juan Yang. "Effect of the BBC3 Gene on the Proliferation and Apoptosis of Hepatocellular Carcinoma Cells Through p53-Regulated Signaling." Journal of Biomaterials and Tissue Engineering 11, no. 1 (January 1, 2021): 135–41. http://dx.doi.org/10.1166/jbt.2021.2386.
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We examined the effect of the BBC3 gene on hyperplasia and apoptosis in HepG2 cells and its underlying mechanism. Quantitative RT-PCR was used to determine the level of BBC3 expression in HL-7702 normal human liver cells and four different hepatocellular carcinoma cell lines (HepG2, HuH-7, HCCLM3 and MHCC97H). Transfection was performed with Lipofectamine 2000 reagent and the transfectants were divided into three groups: pcDNA-BBC3 group (transfected BBC3 over-expressing plasmid), pcDNA-NC group (transfected empty plasmid), and a Ctrl group (not transfected). Quantitative RT-PCR and western blot analysis were used to measure BBC3 expression. The CCK-8 assay was used to determine the effect of BBC3 on HepG2 cell proliferation. Flow cytometry was used for testing the effect of overexpressing BBC3 on apoptosis in HepG2 cells. The levels of cleaved-Caspase-3 (C-Caspase-3), cleaved-Caspase-9 (C-Caspase-9), and proteins associated with the p53 signaling pathway were assessed by western blot analysis. The level of BBC3 mRNA in HL-7702 normal human liver cells was significantly higher compared with that in human hepatocellular carcinoma cells including HepG2, HuH-7, HCCLM3 and MHCC97H (P < 0.05). The lowest level of BBC3 mRNA was observed in HepG2 cells. The level of BBC3 mRNA and protein in HepG2 cells were significantly higher compared with that of the pcDNA-NC group following transfection with a BBC3 overexpressing plasmid. HepG2 cell proliferation in the pcDNA-NC group was higher compared with that of the pcDNA-BBC3-transfected group (P < 0.05). The apoptotic rate and levels of cleaved-Caspase-3, cleaved-Caspase-9, p53, phospho-p53, and p21 protein in cells were higher compared with that of the pcDNA-NC group. No change was observed in the pcDNA-NC and Ctrl groups. The BBC3 gene was down-regulated in hepatocellular carcinoma cells. HepG2 cell proliferation can be inhibited and HepG2 cell apoptosis can be induced by the overexpression of BBC3 through activation of the p53 signaling pathway.
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Tao, Zhengchao, and Liting Qian. "Effect of p53 gene transfection on human hepatocarcinoma cells' sensitivity to irradiation." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e22018-e22018. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22018.
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e22018 Background: Several studies demonstrated that p53 gene transfection enhanced the anti-tumor effects of radiotherapy. This study is to investigate whether p53 gene transfection can increase the radiosensitivity of liver tumor cells. Methods: Liver tumor cell lines, HepG2 (with wild type p53 genes) and PLC/PRF/5 (with mutant p53 genes), were separately transfected with recombinant adenoviral human p53 gene (rAdp53) and adenoviral enhance green fluorescent protein gene (AdEGFP), forming 4 types of cells: HepG2 transfected with rAdp53, HepG2 with AdEGFP, PLC/PRF/5 with rAdp53, and PLC/PRF/5 with AdEGFP. The transfected and untransfected HepG2 and PLC/PRF/5 cells were irradiated with 6MV-X at doses of 0, A2, A4, A6, A8, A and 10 Gy. After exposition to radiation, cell survival, clonogenic capacity, and apoptosis were analyzed. The effect differences between cell types were analyzed using statistical methods of pairwise group comparisons and mixed effect model. Results: After exposing irradiation, all the cells’ survival rate and clonogenic capacity decreased, and the proportion of apoptotic cell increased. These effects become stronger with increaseing dose of radiation. Between untransfected cells, radiation had a stronger effect on HepG2 cells than PLC/PRF/5 and the differences were statistically significant for all the 3 measures. The rAdp53 transfection, not the AdEGFP, significantly enhanced radiation effects on both cell lines. The enhanced effects on PLC/PRF/5 cells were significantly stronger then the enhanced effects on HepG2 cells. Conclusions: PLC/PRF/5 cells with mutant p53 genes were more resistant to radiation then HepG2 with wide type of p53 genes. The rAd-P53 transfection could enhance radiosensitivity of both cell lines, but the enhanced effect on PLC/PRF/5 cells with mutant p53 gene was stronger than HepG2 with wide type of p53 genes.
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Wen, Jinhua, and Menghua Zhao. "OATP1B1 Plays an Important Role in the Transport and Treatment Efficacy of Sorafenib in Hepatocellular Carcinoma." Disease Markers 2021 (September 25, 2021): 1–13. http://dx.doi.org/10.1155/2021/9711179.
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Background. Sorafenib is an anticancer drug used in the treatment of unresectable hepatocellular carcinoma and advanced renal cell carcinoma. It is a substrate for the human OATP1B1. This study is aimed at assessing the role of OATP1B1 in transportation and uptake of sorafenib in hepatocellular carcinoma and how OATP1B1 affects the pharmacodynamics of sorafenib in vitro and in vivo. Methods. Sorafenib transport was measured in HepG2, HepG2-OATP1B1 ∗ 1a, HepG2-OATP1B1 ∗ 1b, HepG2-OATP1B1 ∗ 15, LO2, LO2-OATP1B1 ∗ 1a, LO2-OATP1B1 ∗ 1b, and LO2-OATP1B1 ∗ 15 cells, as well as in HepG2 cells transfected with miR-148a mimics. The viability and apoptosis rate of cells treated with sorafenib were evaluated. A liver cancer rat model was established to explore the pharmacokinetics and pharmacodynamics of sorafenib after overexpression of Oatp2. Results. Changes in expression and genetic mutations of OATP1B1 significantly affected the uptake of sorafenib in HepG2 and LO2 transgenic cells, and the uptake of sorafenib was higher in HepG2 than LO2. Genetic mutations of OATP1B1 significantly affected the cell viability and apoptosis rate of HepG2 cells after sorafenib treatment. Compared to control group, the uptake of sorafenib in miR-148a mimic-transfected HepG2 cells was decreased, and the cell viability was increased. PCN significantly increased the expression of Oatp2 and affected the pharmacokinetics of sorafenib. Vascular endothelial growth factor levels and microvascular density in tumor-adjacent tissues decreased significantly, suggesting that increased Oatp2 expression improves the treatment effect of sorafenib in a rat model of liver cancer. Conclusions. OATP1B1 plays an important role in the pharmacokinetics and pharmacodynamics of sorafenib in hepatocellular carcinoma.
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Shen, Kun-Hung, Zong-Tsi Chen, and Pin-Der Duh. "Cytotoxic Effect of Eucalyptus citriodora Resin on Human Hepatoma HepG2 Cells." American Journal of Chinese Medicine 40, no. 02 (January 2012): 399–413. http://dx.doi.org/10.1142/s0192415x12500310.
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The aim of this study was to evaluate the antiproliferative effect of Eucalyptus citriodora resin (ECR) on human hepatoma HepG2 cells. The results from MTT assay and LDH leakage analysis showed that water extracts of ECR (WEECR) in the dose range of 0–500 μg/ml displayed stronger cytotoxic effects on HepG2 cells than other organic solvent extracts of ECR. By flow cytometry analysis, WEECR slowed down the cell cycle at the G0/G1 phase after 24 h of incubation. Moreover, WEECR treatment induced an apoptotic response in HepG2 cells. WEECR-induced apoptosis was in association with the attenuation of mitochondrial transmembrane potentials (ΔΨ m ), increased Bax/Bcl-2 ratio and activation of caspase-3. In addition, WEECR contained high concentration of phenolics and flavonoids, which may be responsible for the potent cytotoxicity of WEECR on HepG2 cells. Taken together, WEECR may be a potent antihepatoma agent due to apoptosis in HepG2 cells.
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Mee, Christopher J., Helen J. Harris, Michelle J. Farquhar, Garrick Wilson, Gary Reynolds, Christopher Davis, Sven C. D. van IJzendoorn, Peter Balfe, and Jane A. McKeating. "Polarization Restricts Hepatitis C Virus Entry into HepG2 Hepatoma Cells." Journal of Virology 83, no. 12 (April 8, 2009): 6211–21. http://dx.doi.org/10.1128/jvi.00246-09.
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ABSTRACT The primary reservoir for hepatitis C virus (HCV) replication is believed to be hepatocytes, which are highly polarized with tight junctions (TJ) separating their basolateral and apical domains. HepG2 cells develop polarity over time, resulting in the formation and remodeling of bile canalicular (BC) structures. HepG2 cells expressing CD81 provide a model system to study the effects of hepatic polarity on HCV infection. We found an inverse association between HepG2-CD81 polarization and HCV pseudoparticle entry. As HepG2 cells polarize, discrete pools of claudin-1 (CLDN1) at the TJ and basal/lateral membranes develop, consistent with the pattern of receptor staining observed in liver tissue. The TJ and nonjunctional pools of CLDN1 show an altered association with CD81 and localization in response to the PKA antagonist Rp-8-Br-cyclic AMPs (cAMPs). Rp-8-Br-cAMPs reduced CLDN1 expression at the basal membrane and inhibited HCV infection, supporting a model where the nonjunctional pools of CLDN1 have a role in HCV entry. Treatment of HepG2 cells with proinflammatory cytokines, tumor necrosis factor alpha and gamma interferon, perturbed TJ integrity but had minimal effect(s) on cellular polarity and HCV infection, suggesting that TJ integrity does not limit HCV entry into polarized HepG2 cells. In contrast, activation of PKC with phorbol ester reduced TJ integrity, ablated HepG2 polarity, and stimulated HCV entry. Overall, these data show that complex hepatocyte-like polarity alters CLDN1 localization and limits HCV entry, suggesting that agents which disrupt hepatocyte polarity may promote HCV infection and transmission within the liver.
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Nguyen, Sinh Truong. "ID2009 H. Odorata methanol extract inhibits hepatocellular carcinoma HepG2 cells line via induction of caspase-dependent apoptosis." Biomedical Research and Therapy 4, S (September 5, 2017): 42. http://dx.doi.org/10.15419/bmrat.v4is.252.
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Background: Globally cancer is a disease which is major burden to human health nowadays. The demand for new therapies to treat and to prevent cancer disease frequently exists. Since the toxic side effect of current treatment such as chemotherapy, the research interest is paying attention toward naturally derived-compounds because of their selective toxicity to cancer cell. This study aims to test the anticancer activity of a crude extract of Hopea odorata on HepG2 cancer cell line.
Method: Methanol extract were prepared from the bark of H. odorata plant. In vitro cytotoxicity Hopea odorata extract on human hepatocellular carcinoma cell line HepG2, compared to normal human cell fibroblast (HF), was investigated by Alamar Blue assay. Caspase-3/7 was detected using the reagent that consists of DEVD peptide conjugated to a nucleic acid-binding dye. The apoptosis induction of plant extract on HepG2 was recognized by Annexin V/7AAD using flow cytometry. Disintergrated nuclei of plant-treated cell was observed under fluorescent microscope using Hoechst/PI staining. With the same technique of staining, the ratio of dead/total cells was determined by distingusing Hoechst and PI fluorescent signal.
Results. We found that the IC50 value of Hopea odorata extract on HepG2 is at 12.67± 5µg/ml, this value is at 44.2± 3µg/ml on HF. Vice versa, the IC50 value of Doxo on HepG2 153.3±15ng/ml while that is 6.3 ±0.6083ng/ml on HF. The selectivity index of H. Odorata extract (SI) toward HepG2 cells is approximately 3.48, while the SI of Doxorubicin toward HepG2 cells is approximately 0.04. The ratio of dead/total cells increased in dose-dependent manner when observed under fluorescent microscope, while the ratio of dead/total cells barely changed on HF cells. The plant extract inhibited HepG2 through the activation of caspase-3/7. At the concentration 250µg/ml of plant extract, 35% HepG2 cells was induced into apoptosis, and HepG2 cells appeared with disintegrated nuclei under fluorescent microscope.
Conclusion. These finding showed methanolic extract of Hopea odorata plant induced apoptosis and selectively cytotoxic toward HepG2 rather than human fibroblast cells. Purification of compounds from Hopea odorata extract need to be performed for further research the anticancer properties of Hopea odorata.
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Said, Hamid M., Svetlana M. Nabokina, Krishnaswamy Balamurugan, Zainab M. Mohammed, Cecilia Urbina, and Moti L. Kashyap. "Mechanism of nicotinic acid transport in human liver cells: experiments with HepG2 cells and primary hepatocytes." American Journal of Physiology-Cell Physiology 293, no. 6 (December 2007): C1773—C1778. http://dx.doi.org/10.1152/ajpcell.00409.2007.
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This study reports on the functional expression of a specific, high-affinity carrier-mediated mechanism for the transport of niacin (nicotinic acid) in human liver cells. Both human-derived liver HepG2 cells and human primary hepatocytes were used as models in these investigations. The initial rate of transport of nicotinic acid into HepG2 cells was found to be acidic pH, temperature, and energy dependent; it was, however, Na+ independent in nature. Evidence for the existence of a carrier-mediated system that is specific for [3H]nicotinic acid transport was found and included the following: 1) saturability as a function of concentration with an apparent Km of 0.73 ± 0.16 μM and Vmax of 25.02 ± 1.45 pmol·mg protein−1·3 min−1, 2) cis-inhibition by unlabeled nicotinic acid and nicotinamide but not by unrelated organic anions (lactate, acetate, butyrate, succinate, citrate, and valproate), and 3) trans-stimulation of [3H]nicotinic acid efflux by unlabeled nicotinic acid. Transport of the vitamin into human primary hepatocytes occurs similarly via an acidic pH-dependent and specific carrier-mediated process. Inhibitors of the Ca2+-calmodulin-mediated pathway (but not modulators of the PKC-, PKA-, and protein tyrosine kinase-mediated pathways) inhibited nicotinic acid transport into both HepG2 cells and human primary hepatocytes. Maintenance of HepG2 cells (for 48 h) in growth medium oversupplemented with nicotinic acid (or nicotinamide) did not affect the subsequent transport of [3H]nicotinic acid into HepG2 cells. These results show, for the first time, the existence of a specific and regulated membrane carrier-mediated system for nicotinic acid transport in human liver cells.
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Yu, Dan, Jin Xu, Ya Chen, and Bimin Shi. "Procyanidin A1 Inhibits Insulin Resistance and Oxidative Stress in Palmitic Acid Treated HepG2 Cells." Current Topics in Nutraceutical Research 20, no. 3 (March 16, 2022): 561–66. http://dx.doi.org/10.37290/ctnr2641-452x.20:561-566.
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The present study has examined the effect of procyanidin A1 on insulin resistance and oxidative stress in palmitic acid treated HepG2 cells. The HepG2 cells were pretreated with procyanidin A1 and then with palmitic acid. The cell viability and the levels of catalase, superoxide dismutase, glutathione peroxidase, and reactive oxygen were used to assess oxidative stress. Treatment with palmitic acid significantly reduced cell viability that was alleviated by cotreatment with procyanidin A1. In addition, procyanidin A1 restored the palmitic acid induced insulin resistance and oxidative stress in the HepG2 cells. Furthermore, inactivation of P38 MAPK and JNK signaling pathways was closely associated with the procyanidin A1-regulated resistance and oxidative stress in palmitic acid treated HepG2 cells. In conclusion, procyanidin A1 inhibits insulin resistance and oxidative stress in palmitic acid treated HepG2 cells by regulating the P38 MAPK and JNK signaling pathways.
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Buchner, R. R., T. E. Hugli, J. A. Ember, and E. L. Morgan. "Expression of functional receptors for human C5a anaphylatoxin (CD88) on the human hepatocellular carcinoma cell line HepG2. Stimulation of acute-phase protein-specific mRNA and protein synthesis by human C5a anaphylatoxin." Journal of Immunology 155, no. 1 (July 1, 1995): 308–15. http://dx.doi.org/10.4049/jimmunol.155.1.308.
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Abstract Acute inflammation is characterized by increased production of acute phase proteins in the liver. The induction of the hepatocytic response is primarily mediated through soluble cytokines such as IL-1, IL-6, TNF-alpha, and transforming growth factor beta, which bind to specific cell surface receptors and regulate gene expression of acute-phase proteins. Hepatoma cell lines, such as HepG2, represent a model system for studying acute-phase protein synthesis. HepG2 is induced to produce a variety of acute-phase proteins, including alpha 1-antitrypsin, alpha 1-antichymotrypsin, fibrinogen, alpha 1-acid glycoprotein, and haptoglobin, upon stimulation with cytokines. Analysis of HepG2 by reverse transcriptase PCR indicated that this cell line synthesized mRNA specific for the human C5a receptor (CD88). Flow cytometric analysis of HepG2 cells indicated that these cells bound anti-CD88 Ab, thus confirming our RT-PCR data by demonstrating that these cells also express the C5a receptor. Because C5a has been shown to be a potent mediator of inflammation and HepG2 cells express CD88, we assessed the possibility that C5a was capable of stimulating acute-phase protein synthesis by HepG2 cells. The results indicate that binding of human C5a to CD88 on HepG2 cells resulted in an increased production of alpha 1-antitrypsin- and alpha 1-antichymotrypsin-specific mRNA as assayed by RT-PCR. Analysis of culture supernatants derived from C5a-stimulated HepG2 cells showed an increased production of alpha 1-antitrypsin as measured by solid-phase ELISA. alpha 1-antitrypsin production by HepG2 cells was a direct result of C5a stimulation as evidenced by the fact that anti-C5a receptor Ab inhibited the response. These results suggest that C5a may be an important mediator of APP production in the regulation of the inflammatory response.
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Nguyen, Sinh Truong, Nghia Minh Do, Phuc Hong Vo, Trinh Thi –. Tu Nguyen, Kiet Dinh Truong, and Phuc Van Pham. "Xao tam phan (Paramignya trimera) methanol extract induced apoptosis in hepatocellular carcinoma HepG2 cell line in vitro." Science and Technology Development Journal 23, no. 1 (March 31, 2020): 484–89. http://dx.doi.org/10.32508/stdj.v23i1.2013.
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Introduction: Xao Tam Phan (Paramignya trimera) has long been used in Viet Nam as an herbal medicine for the treatment of Hepatitis, hepatocellular carcinoma, and diabetes. This study aimed to determine the anti-proliferation effect of Paramignya trimera extract (P. trimera extract) on HepG2 hepatocellular carcinoma cells.
Methods: AlamarBlue assay was used to determine the IC50 values of P. trimera extract on HepG2 cells. Adipose-derived stem cells (ADSCs) was used as normal cell control. For apoptosis examination, P. trimera extract-treated HepG2 cells were incubated with Annexin V/Propidium iodide (PI). Then they have been analyzed their expression of Annexin-V and PI by flow cytometry. The cell nuclear degradation also was evaluated by PI/Hoechst 33342 staining assay.
Results: Doxorubicin and P. trimera extract IC50 values on HepG2 cells were 55.13 +/- 2.028 ng/ml and 582.533 +/- 16.521 mg/ml, respectively. Those on ADSCs were 5.96 +/- 0.56 ng/ml and 268.976 +/- 19.325 mg/ml, respectively. Side effect index value (SEI) of P. trimera extract was 2.175 +/- 0.12, and the SEI of doxorubicin was 8.71 +/- 0.36. Flow cytometry analysis indicated significant apoptosis on P. trimera extract-treated HepG2 cells at a dose of 500 mg/ml (32.39 +/- 2.28% apoptotic cells, and 14.63 +/- 1.59% necrotic cells). Nuclear aggregation and degradation was seen on 500 mg/ml P. trimera treated HepG2 cells.
Conclusion: P. trimera extract could inhibit HepG2 hepatocellular carcinoma cell proliferation by inducing apoptosis.