Journal articles on the topic 'HCT-116 cells'
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1
Luminturahardjo, Winarko, Djoko Wahono Soeatmadji, Karyono Mintaroem, Pudji Rahajoe, and Ferry Sandra. "N-Cadherin as An Important Marker in Colorectal Cancer: An investigation of b-Catenin and Cadherin Expressions of SW-480 and HCT-116 Cell Lines." Indonesian Biomedical Journal 13, no. 3 (September 9, 2021): 289–94. http://dx.doi.org/10.18585/inabj.v13i3.1562.
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BACKGROUND: The absence of potential biomarkers to detect the metastatic process at an early stage will consequently delay colorectal cancer (CRC) treatment. Some biomarkers including β-Catenin, E-Cadherin and N-Cadherin have been suggested as potential markers. However, there were opposite reports regarding expressions of these markers. Therefore, current study was conducted using CRC cell lines for early stage (SW-480 cells) and late stage (HCT-116 cells) of CRC.METHODS: SW-480 and HCT-116 cells were cultured and seeded on coverslip glasses for immunofluorescence staining to detect β-Catenin, E-cadherin, and N-cadherin. Expressions of β-Catenin, E-cadherin, and N-cadherin were observed and documented under a fluorescent microscope and analyzed with Image J software. Measured results were then statistically analyzed. RESULTS: All β-catenin, E-Cadherin and N-Cadherin expressions were observed in SW-480 and HCT-116 cells. β-catenin MFI averages of SW-480 (47.157±3.479) and HCT-116 (47.240±4.107) cells were similar. E-Cadherin MFI average of SW-480 cells (45.104±4.107) was higher than the one of HCT-116 cells (40.191±3.702). N-Cadherin MFI average of HCT-116 cells (43.702±8.219) was significantly higher (p=0.009) than the one of SW-480 cells (72.506±5.297).CONCLUSION: Taken together, N-Cadherin could be suggested as an important metastasis marker in CRC since the N-Cadherin expression was significantly higher in HCT-116 cells as the late-stage CRC model than SW-480 as the early-stage of CRC model. Further research is still needed by comparing several biomarkers from various clinical samples at all clinical stages of CRC.KEYWORDS: CRC, β-Catenin, E-Cadherin, N-Cadherin, Metastasis, Biomarker
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Hsieh, Shu-Ling, Shuchen Hsieh, Yu-Hao Kuo, Jyh-Jye Wang, Jinn-Chyi Wang, and Chih-Chung Wu. "Effects of Panax notoginseng on the Metastasis of Human Colorectal Cancer Cells." American Journal of Chinese Medicine 44, no. 04 (January 2016): 851–70. http://dx.doi.org/10.1142/s0192415x16500476.
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The goal of this study was to investigate the effect of the Panax notoginseng ethanol extract (PNEE) on the regulation of human colorectal cancer (CRC) metastasis. The migratory, invasive, and adhesive abilities and the expression of metastasis-associated regulatory molecules in cultured human CRC cells (HCT-116) treated with the PNEE were analyzed in this study. The migratory and invasive abilities of HCT-116 cells were reduced after PNEE treatment. The incubation of HCT-116 cells with the PNEE for 24 h decreased MMP-9 expression and increased E-cadherin expression compared with the control group. The adhesion reaction assay indicated that treatment with the PNEE led to significantly decreased HCT-116 adhesion to endothelial cells (EA.hy926 cells). The integrin-1 protein levels in HCT-116 cells were significantly decreased following treatment with the PNEE. Similarly, the protein levels of E-selectin and intercellular adhesion molecule-1 (ICAM-1) were significantly decreased by treatment of the EA.hy926 endothelial cells with PNEE. A scanning electron microscope (SEM) examination indicated that HCT-116 cells treated with LPS combined with the PNEE had a less flattened and retracted shape compared with LPS-treated cells, and this change in shape was found to be a phenomenon of extravasation invasion. The transepithelial electrical resistance (TEER) of the EA.hy926 endothelial cell monolayer increased after incubation with the PNEE for 24 h. A cell-cell permeability assay indicated that HCT-116 cells treated with the PNEE displayed significantly reduced levels of phosphorylated VE-cadherin (p-VE-cadherin). These results demonstrate the antimetastatic properties of the PNEE and show that the PNEE affects cells by inhibiting cell migration, invasion, and adhesion and regulating the expression of metastasis-associated signaling molecules.
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Leong, Lek Mun, Kok Meng Chan, Asmah Hamid, Jalifah Latip, and Nor Fadilah Rajab. "Herbal Formulation C168 Attenuates Proliferation and Induces Apoptosis in HCT 116 Human Colorectal Carcinoma Cells: Role of Oxidative Stress and DNA Damage." Evidence-Based Complementary and Alternative Medicine 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/2091085.
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The use of herbal formulations has gained scientific interest, particularly in cancer treatment. In this study, the herbal formulation of interest, denoted as C168, is a mixture of eight genera of plants. This study aims to investigate the antiproliferative effect of C168 methanol extract (CME) on various cancer cells and its underlying mechanism of action on the most responsive cell line, namely, HCT 116 cells. CME exerted antiproliferative activities on HCT 116 colorectal carcinoma cells and HepG2 hepatocellular carcinoma cells but not on CCD-841-CoN normal colon epithelial cells, Jurkat E6.1 lymphoblastic leukemic cells, and V79-4 Chinese hamster lung fibroblasts. Further investigation on HCT 116 cells showed that CME induced G2/M cell-cycle arrest and apoptosis. Treatment of CME induced oxidative stress in HCT 116 cells by increasing the superoxide anion level and decreasing the intracellular glutathione. CME also increased tail moment value and H2AX phosphorylation in HCT 116 cells, suggesting DNA damage as an early signal of CME induced apoptosis. Loss of mitochondrial membrane potential in CME-treated cells also indicated the involvement of mitochondria in CME induced apoptosis. This study indicated the selectivity of CME toward colon cancer cells with the involvement of oxidative damage as its possible mechanism of action.
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Wu, Peng, Ting Yu, Jun Wu, and Junfeng Chen. "Licochalcone a Induces ROS-Mediated Apoptosis through TrxR1 Inactivation in Colorectal Cancer Cells." BioMed Research International 2020 (May 28, 2020): 1–11. http://dx.doi.org/10.1155/2020/5875074.
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Licochalcone A (LCA) exhibited anticancer activity through modulating reactive oxygen species (ROS) levels in some cancer cells and has been evidenced to suppress colorectal cancer (CRC) formation and progression. However, whether LCA mediates the progression of CRC by regulating ROS production remains unclear. To address this, HCT-116 cells were treated with LCA, resulting in G0/G1 phase arrest, apoptosis, and high ROS generation, which were attenuated by N-acetyl-L-cysteine, a ROS inhibitor. In addition, LCA suppressed the expression of thioredoxin reductase 1 (TrxR1) in HCT-116 cells, leading to high ROS levels and apoptosis. Moreover, LCA administration combined with TrxR1 inhibition further enhanced the production of ROS and apoptosis in HCT-116 cells compared to LCA administration or TrxR1 inhibition alone. These results demonstrated that LCA might enhance the production of ROS by targeting TrxR1, leading to apoptosis in HCT-116 cells, which provides potential insight for the interventional treatment of CRC.
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Huang, Ya-Li, Fang Wei, Ke Zhao, Yong Zhang, Dong Wang, and Xin-Hua Li. "Isoliquiritigenin inhibits colorectal cancer cells HCT-116 growth by suppressing the PI3K/AKT pathway." Open Life Sciences 12, no. 1 (October 23, 2017): 300–307. http://dx.doi.org/10.1515/biol-2017-0035.
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AbstractIsoliquiritigenin (ISL), a member of the flavonoids, is known to possess antitumor activity in different types of cancer including human breast cancer, hepatoma cancer, prostate cancer and others, bothin vitroandin vivo. In the present study, we reported the effect of ISL on cell growth in human colorectal cancer cells HCT-116. As examined by CCK8 assays, ISL inhibited the proliferation of HCT-116 cells. Additionally, the antimigratory activity of ISL in HCT-116 cells was confirmed by trans-well chamber migration assays and invasion assays. Moreover, the results of fluorescence-activated cell sorting and Sodium Dodecyl Sulfate-Polyacrylamide Gel Electrophoresis (SDS-PAGE) analysis showed that ISL induced apoptosis in HCT-116 cells. Further detection using SDS-PAGE assay revealed that ISL decreased the levels of phospho-AKT (p-AKT), phospho-mTOR (p-mTOR), Cyclin D1 and phospho-p70S6 Kinase (p-P70S6K). Collectively, these findings indicated that isoliquiritigenin induced growth-inhibition and apoptosis through downregulating of PI3K/AKT in human colorectal cancer.
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Masese Osoro Brian and Selvi S. "Cytotoxic effects of Ceiba pentandra L. mediated silver nanoparticles on HCT-116 colon cancer cell lines through ROS generation and cell membrane damage." International Journal of Research in Pharmaceutical Sciences 10, no. 4 (October 16, 2019): 3236–43. http://dx.doi.org/10.26452/ijrps.v10i4.1627.
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In this study, we assessed the biological effect of Ceiba pentandra bark silver nanoparticles (CP-AgNPs) on HCT-116 cancer cells with an emphasis on cell cytotoxicity, quantification of ROS and determination of mitochondria membrane potential. The synthesized Ceiba pentandra bark silver nanoparticles were characterized by UV-vis spectrometer, High-resolution transmission electron microscope (HR-TEM), X-ray diffraction (XRD) and Selected area electron diffraction (SAED). The synthesized silver nanoparticle cytotoxic and apoptotic effects were studied on colorectal cancer cells (HCT-116). The nanoparticles exhibited an inhibitory concentration (IC50) at (60μg/mL). CP-AgNPs significantly inhibited cell viability and changed the morphology of HCT-116 colon cancer cells. Moreover, CP-AgNPs increased the level of reactive oxygen species, induced cell apoptosis in HCT-116 cell lines through the interference of the mitochondrial membrane potential. These results indicated that Ceiba pentandra bark silver nanoparticles (CP-AgNPs) might act as prospective anticancer agents in colon cancer cells.
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Bian, Zhongbo, Xiaodie Sun, Lulin Liu, Yong Qin, Qiuyu Zhang, Huahuan Liu, Lianzhi Mao, and Suxia Sun. "Sodium Butyrate Induces CRC Cell Ferroptosis via the CD44/SLC7A11 Pathway and Exhibits a Synergistic Therapeutic Effect with Erastin." Cancers 15, no. 2 (January 9, 2023): 423. http://dx.doi.org/10.3390/cancers15020423.
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Colorectal cancer (CRC) is one of the most common malignancies, and effective treatment and prevention methods are lacking. Sodium butyrate (NaB) is a short-chain fatty acid produced by intestinal microbial fermentation of dietary fiber. It has been shown to be effective in inhibiting CRC, but the mechanism is not known. Methods: Human normal intestinal epithelial cell line FHT and colorectal tumor cell line HCT-116 were treated with NaB alone or in combination with different programmed cell death inhibitors. Cell activity was then assessed with MTT assays and PI staining; ferroptosis with Fe2+, glutathione (GSH), and lipid peroxidation assays; signaling pathway screening with PCR arrays; and CD44, SCL7A11, and GPX4 expression with Western blotting. A CD44-overexpressing HCT-116 cell line was constructed to determine the effect of the overexpression of CD44 on NaB-induced ferroptosis. The synergistic effect of co-treatment with NaB and Erastin was assessed by isobolographic analysis. Results: NaB induced apoptosis and ferroptosis in HCT-116 cells but only induced low-level apoptosis in FHC cells. Moreover, NaB significantly increased intracellular Fe2+ and promoted GSH depletion and lipid peroxidation in HCT-116 cells. Ferroptosis-related qPCR array analysis identified CD44/SLC7A11 as a potential effector molecular of NaB-induced ferroptosis. NaB significantly inhibited the expression of CD44 and SLC7A11 in mouse CRC tissues. A CD44 overexpressed HCT-116 cell line was used to verify that CD44/SLC7A11 was a key signaling pathway that NaB-induced GSH depletion, lipid peroxidation accumulation, and ferroptosis in HCT-116 cells. Examination of whether NaB can increase the effect of ferroptosis agents showed that NaB, in combination with Erastin, a ferroptosis inducer, further promoted HCT-116 cell death and increased changes of ferroptosis markers. Conclusions: Our results suggest that NaB induces ferroptosis in CRC cells through the CD44/SLC7A11 signaling pathway and has synergistic effects with Erastin. These results may provide new insights into CRC prevention and the combined use of NaB and ferroptosis-inducing agents.
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Kırımtay, Koray, Ece Selçuk, Dolunay Kelle, Batu Erman, and Arzu Karabay. "p53 regulates katanin-p60 promoter in HCT 116 cells." Gene 727 (February 2020): 144241. http://dx.doi.org/10.1016/j.gene.2019.144241.
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Zhang, Haiying, Jianan Sun, Ruoting Ma, and Shengjun Zhao. "Role of Episamarcandin in Promoting the Apoptosis of Human Colon Cancer HCT116 Cells through the PI3K-Akt Signaling Pathway." Evidence-Based Complementary and Alternative Medicine 2021 (November 2, 2021): 1–12. http://dx.doi.org/10.1155/2021/9663738.
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This study identifies the active ingredients of Ferula sinkiangensis and investigates the role and mechanism of episamarcandin in colon cancer cells. The silica gel column chromatography was utilized to separate the chemical components of Ferula sinkiangensis. Sephadex LH-20 and semipreparative HPLC were adopted for further separation and purification. The compound episamarcandin showed good anticolon cancer activity among the 13 monomeric compounds obtained. Its effects on the apoptosis, cell cycle, and invasion and migration of colon cancer HCT 116 cells and PI3K-Akt signaling pathway were further investigated. The results showed that, similar to positive control cisplatin, episamarcandin inhibited the proliferation, promoted the apoptosis, arrested cells at G0/G1 phase, and suppressed migration and invasion of HCT 116 cells. A large number of apoptotic HCT 116 cells were observed under a transmission electron microscope. Fluorescence real-time quantitative PCR and western blot analysis showed that episamarcandin increased the expression of PTEN, p53, and Bax and decreased the expression of P-Akt, Akt, mTOR, Bcl-xl, and Bcl-2. Conclusively, episamarcandin may inhibit cell proliferation, migration, and invasion and promote the apoptosis of human colon cancer HCT 116 cells possibly through the PI3K-Akt signaling pathway.
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Apaydin Yildirim Betul. "Anti-cancer, antiproliferative activity of active anionic H2O8 oxygen solution on HCT-116 cancer cell." World Journal of Advanced Research and Reviews 12, no. 2 (November 30, 2021): 179–84. http://dx.doi.org/10.30574/wjarr.2021.12.2.0560.
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HCT116 cells are adherent epithelial cells derived from the human colorectal carcinoma cell line commonly used to study inflammatory responses in colonic epithelial cells. In this study, it was aimed to evaluate the effects of active anionic H2O8 oxygen solution, which is a very strong antiviral and antimicrobial agent, on HCT-116 human colorectal cancer cell line. Cell viability was determined by MTT analysis. Antiproliferative activity of the anionic H2O8 was investigated on HCT 116 (human colorectal carcinoma) cancer cells. Anionic H2O8 displayed the outstanding activities for MTT test, IC50= 9.44 for 24th hour was calculated as IC50= 11.73 for 48th hour on HCT 116 cell line. It is thought that it can serve as an agent with strong potential to be used in treatment.
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El-Sayed, Nahed N. E., Magdi E. A. Zaki, Sami A. Al-Hussain, Abir Ben Bacha, Malika Berredjem, Vijay H. Masand, Zainab M. Almarhoon, and Hanaa S. Omar. "Synthesis and Evaluation of Some New 4H-Pyran Derivatives as Antioxidant, Antibacterial and Anti-HCT-116 Cells of CRC, with Molecular Docking, Antiproliferative, Apoptotic and ADME Investigations." Pharmaceuticals 15, no. 7 (July 19, 2022): 891. http://dx.doi.org/10.3390/ph15070891.
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Colorectal cancer oncogenesis is linked to dysbiosis, oxidative stress and overexpression of CDK2. The 4H-pyran scaffold is considered an antitumoral, antibacterial and antioxidant lead as well as a CDK2 inhibitor. Herein, certain 4H-pyran derivatives were evaluated as antibacterial, antioxidant and cytotoxic agents against HCT-116 cells. Derivatives 4g and 4j inhibited all the tested Gram-positive isolates, except for B. cereus (ATCC 14579), with lower IC50 values (µM) than ampicillin. In addition, 4g and 4j demonstrated the strongest DPPH scavenging and reducing potencies, with 4j being more efficient than BHT. In cell viability assays, 4d and 4k suppressed the proliferation of HCT-116 cells, with the lowest IC50 values being 75.1 and 85.88 µM, respectively. The results of molecular docking simulations of 4d and 4k, inhibitory kinase assays against CDK2, along with determination of CDK2 protein concentration and the expression level of CDK2 gene in the lysates of HCT-116 treated cells, suggested that these analogues blocked the proliferation of HCT-116 cells by inhibiting kinase activity and downregulating expression levels of CDK2 protein and gene. Moreover, 4d and 4k were found to induce apoptosis in HCT-116 cells via activation of the caspase-3 gene. Lastly, compounds 4g, 4j, 4d and 4k were predicted to comply with Lipinski’s rule of five, and they are expected to possess excellent physiochemical and pharmacokinetic properties suitable for in vivo bioavailability, as predicted by the SwissADME web tool.
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Wang, Yu-Xuan, Cheng Lin, Lu-Jia Cui, Wan-He Yang, Qiu-Min Li, Zhan-Ju Liu, and Xin-Pu Miao. "Rauwolfia vomitoria Extract Represses Colorectal Cancer Cell Autophagy and Promotes Apoptosis." Pharmacology 106, no. 9-10 (2021): 488–97. http://dx.doi.org/10.1159/000512614.
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<b><i>Background:</i></b> Colorectal cancer (CRC) is one of the most frequent digestive tract tumors in the world with an increasing incidence. Currently, surgical resection and chemotherapy are the main therapeutic options; however, their effects are limited by various adverse reactions. <i>Rauwolfia vomitoria</i> extract (Rau) has been shown to repress the progression of multiple human cancers; however, whether Rau plays a role in CRC remains undetermined. <b><i>Methods:</i></b> Influences of Rau treatment on HCT-116 and LoVo cells were estimated via MTT and colony formation experiments. Flow cytometry analysis was adopted to evaluate the apoptosis rate of HCT-116 and LoVo cells. Apoptosis-related proteins (Bcl-2, Bax, and caspase-3) and autophagy-related proteins (LC3 and P62) were assessed by Western blotting. Effects of Rau on autophagy of HCT-116 and LoVo cell were evaluated through GFP-LC3 analysis. In vivo xenograft tumor assay was conducted to further examine the role of Rau in CRC tumor growth. <b><i>Results:</i></b> Rau remarkably repressed HCT-116 and LoVo cell viability and promoted HCT-116 and LoVo cell apoptosis in vitro in a dose-dependent manner. Rau increased the expression of caspase-3 and Bax and decreased the expression of Bcl-2 in HCT-116 and LoVo cells. Moreover, Rau was demonstrated to decrease the LC3||/LC3| ratio and increase the level of P62 in HCT-116 and LoVo cells. In addition, we found that Rau repressed xenograft tumor growth and also repressed autophagy in vivo. <b><i>Conclusion:</i></b> Our findings revealed that Rau repressed CRC cell viability and autophagy in vitro and in vivo, suggesting that Rau might be a potent therapeutic agent of CRC.
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Hsieh, Shu-Ling, ShuChen Hsieh, Po-Yu Lai, Jyh-Jye Wang, Chien-Chun Li, and Chih-Chung Wu. "Carnosine Suppresses Human Colorectal Cell Migration and Intravasation by Regulating EMT and MMP Expression." American Journal of Chinese Medicine 47, no. 02 (January 2019): 477–94. http://dx.doi.org/10.1142/s0192415x19500241.
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Carnosine is an endogenous dipeptide found in the vertebrate skeletal muscles that is usually obtained through the diet. To investigate the mechanism by which carnosine regulates the migration and intravasation of human colorectal cancer (CRC) cells, we used cultured HCT-116 cells as an experimental model in this study. We examined HCT-116 cell migratory and intravasive abilities and expression of epithelial-mesenchymal transition (EMT)-associated molecules and matrix metalloproteinases (MMPs) after carnosine treatment. The results showed that both migration and invasion were inhibited in cells treated with carnosine. We found significant decreases in Twist-1 protein levels and increases in E-cadherin protein levels in HCT-116 cells after carnosine exposure. Although plasminogen activator (uPA) and MMP-9 mRNA and protein levels were decreased, TIMP-1 mRNA and protein levels were increased. Furthermore, the cytosolic levels of phosphorylated I[Formula: see text]B (p-I[Formula: see text]B) and NF-[Formula: see text]B DNA-binding activity were reduced after carnosine treatment. These results indicate that carnosine inhibits the migration and intravasation of human CRC cells. The regulatory mechanism may occur by suppressing NF-[Formula: see text]B activity and modulating MMP and EMT-related gene expression in HCT-116 cells.
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Rostamzadeh Khameneh, Zakieh, Mahshid Mohammadian, Mohammad Aziz Rasouli, Zhino Moradi, Zohre Ahmadi, and Azim Akbarzadeh Khiyavi. "Effects of Curcumin in Combination with Doxorubicin in Human Colorectal Cancer Cell Line." Asian Pacific Journal of Cancer Biology 3, no. 4 (January 3, 2019): 89–92. http://dx.doi.org/10.31557/apjcb.2018.3.4.89-92.
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Background: Colorectal cancer (CRC) is one of the main cause of cancer related death worldwide. New therapeutic strategies are required for CRC. Anthracycline drugs such as doxorubicin (DOX) remain one of the most active wide-spectrum and cost-effective drugs in cancer therapy. However, colorectal cancer (CRC) cells are inherently resistant to anthracyclines. Curcumin, the active component and yellow pigment, has been considered as anti-cancer agents with anti-proliferation, anti-invasion, and anti-angiogenesis properties. Previous data show that curcumin may played main role as therapeutic agent for CRC. We aimed to assess the possible sensitizing effects of curcumin in HCT-116 CRC cells treated with DOX.Methods: HCT-116 cells were treated with different doses of curcumin and DOX in increasing concentrations and cytotoxicity were evaluated after 48 h by Water Soluble Tetrazolium Salts(WST-1) method. In double combination treatments (48 h), the mentioned concentration were utilized; D ( Curcumin; 20 μM;DOX;5μM) C (Curcumin; 10 μM;DOX ;2.5μM ), B (Curcumin; 5 μM;DOX;1μM) and A (Curcumin; 2.5 μM;DOX;0.5μM).Results: HCT-116 cells treatments with various concentrations of single agents (DOX and curcumin) decreased the cellular viability in a dose-dependent pattern. Here, we show that treatment of HCT-116 CRC cells with curcumin increases the efficacy of DOX-induced death in HCT-116 cells. Curcumin treatments also results in higher cytotoxicity of DOX and the cell death percent in compared to higher doses in single treatments.Conclusion: It could be concluded that curcumin could acts as chemosensitiser towards the DOX therapy. So it might be used as adjuvant therapy to enhance DOX sensitivity in CRC cells.
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Kehagias, Pashalina, Nadège Kindt, Mohammad Krayem, Ahmad Najem, Giulia Agostini, Elena Acedo Reina, Giacomo Bregni, et al. "Regorafenib Induces Senescence and Epithelial-Mesenchymal Transition in Colorectal Cancer to Promote Drug Resistance." Cells 11, no. 22 (November 18, 2022): 3663. http://dx.doi.org/10.3390/cells11223663.
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Potential intrinsic resistance mechanisms to regorafenib were explored after short exposure (3 days) on five CRC cell lines (HCT-116, SW1116, LS-1034, SW480, Caco-2). The observation of senescence-like features led to the investigation of a drug-initiated phenotype switch. Following long-term exposure (12 months) of HCT-116 and SW480 cell lines to regorafenib, we developed resistant models to explore acquired resistance. SW480 cells demonstrated senescent-like properties, including a cell arrest in the late G2/prophase cell cycle stage and a statistically significant decrease in the expression of G1 Cyclin-Dependent Kinase inhibitors and key cell cycle regulators. A specific senescence-associated secretome was also observed. In contrast, HCT-116 treated cells presented early senescent features and developed acquired resistance triggering EMT and a more aggressive phenotype over time. The gained migration and invasion ability by long-exposed cells was associated with the increased expression level of key cellular and extracellular EMT-related factors. The PI3K/AKT pathway was a significant player in the acquired resistance of HCT-116 cells, possibly related to a PI3KCA mutation in this cell line. Our findings provide new insights into the phenotypic plasticity of CRC cells able, under treatment pressure, to acquire a stable TIS or to use an early senescence state to undergo EMT.
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Maqbool, Raihana, Saife Niaz Lone, and Mahboob Ul Hussain. "Post-transcriptional regulation of the tumor suppressor p53 by a novel miR-27a, with implications during hypoxia and tumorigenesis." Biochemical Journal 473, no. 20 (October 11, 2016): 3597–610. http://dx.doi.org/10.1042/bcj20160359.
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The tumor suppressor protein p53 is intricately regulated by various signaling molecules, including non-coding small RNAs, called microRNAs (miRNAs). The in silico analysis and the inverse expression status in various cell lines raised the possibility of miR-27a being a new regulator of p53. Using luciferase reporter assay and various mutational and functional analysis, we identified two putative binding sites of miR-27a on the 3′-UTR of p53. The overexpression of miR-27a in the human colorectal cancer cell line HCT-116+/+ resulted in the decreased expression of the endogenous p53 protein levels. During hypoxia of the HCT-116+/+ cells, p53 showed increased accumulation after 3 h, and the levels were significantly up-regulated until 24 h of hypoxia. The p53 expression dynamics during hypoxia of the HCT-116+/+ cells were found to be inversely regulated by miR-27a expression. Moreover, using a cell viability assay, we established that after 3 h of hypoxia, the accumulation of p53 results in a decreased number of the viable HCT-116+/+ cells and the overexpression of miR-27a resulted in an increased number of viable HCT-116+/+ cells with a concomitant decrease in p53 expression. Additionally, our data indicated that miR-27a and p53 depict inverse expression dynamics in 50% of the human colorectal cancer samples studied, when compared with that in the adjacent normal samples. Our data established that miR-27a and the tumor suppressor protein p53 are part of the same signaling network that has important implications during hypoxia and tumorigenesis.
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Yakkanti, Raja Ratna Reddy, P. Chandra Sekhar, K. Bharath Nandhan Reddy, S. Ramamoorthy, S. Ranga Suresh, T. Yasodha Lakshmi, Mani Rajesh, and C. Damodar Reddy. "Limonene and BEZ 235 inhibits growth of COLO-320 and HCT-116 colon cancer cells." International Journal of Drug Delivery 8, no. 3 (December 8, 2016): 89. http://dx.doi.org/10.5138/09750215.1919.
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<p>D-Limonene is a dietary monoterpene with significant anticancer activity against many cancer types in preclinical and clinical studies. The study is designed to investigate synergistic anticancer effects of limonene and BEZ235 combination in COLO-320 and HCT-116 colon cancer cells. Cells were treated with both the drugs alone and in combination and the effects on cell viability; cell migration and clonogenic potential were examined. Results show that both drugs exhibited dose and time dependant cytotoxicity on the cell lines tested. CompuSyn analysis of the drug combination effects revealed the strong synergistic interaction of the combination. Our results also indicate that COLO-320 cells were more sensitive for anticancer effects of the drugs than HCT-116 cells. The presence of Ras and PI3K mutations in HCT-116 cells could possibly be one of the main reasons for the observed outcome as compared to the wild type expressions of them in COLO-320 cells.</p>
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Lai, Po-Yu, Shu-Chen Hsieh, Chih-Chung Wu, and Shu-Ling Hsieh. "ID: 1029 Effects of carnosine on regulation of migration and invasion in human colorectal cancer cells." Biomedical Research and Therapy 4, S (September 5, 2017): 104. http://dx.doi.org/10.15419/bmrat.v4is.305.
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Colorectal cancer is the third most commonly diagnosed cancer in the word. Carnosine is an endogenous dipeptide found in vertebrate skeletal muscles. It is known to have anti-fatigue, antioxidative, antihypertensive, antidiabetic, and cancer inhibiting effects. However, little research has been done regarding its influence on the metastasis of colon cancer. This study cultivated HCT-116 human colon cancer cells as a test model in order to investigate the impact of carnosine on the migration and invasion of human colon cancer cells. The results showed that 48-hour treatments of HCT-116 cells with 0.5, 1, or 5 mM carnosine each significantly inhibited the migration ability of the cells (P < 0.05). The 48-hour treatments with 0.5, 1, or 5 mM carnosine were also found to significantly reduce MMP-9 activity (P < 0.05), but not MMP-2 expression. Furthermore, when HCT-116 cells treated with 1 or 5 mM carnosine, invasion ability are significantly decreased and significantly increased E-cadherin expression (P < 0.05). On the other hand, the protein of TIMP-1, an inhibitor of MMP-9, is signification increased after 1 or 5 mM carnosine treatment (P<0.05). In addition, the u-PA protein level are significantly decreased after carnosine treatment.
The results indicate that carnosine can regulate the migration and invasion by regulating MMPs and its regulator molecular expression in HCT-116 cells.
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Dogan Tuba, Ozturk Serdar, and Apaydin Yildirim Betul. "In vitro anticancer and antiproliferative activity of crocin on HCT-116 cells." World Journal of Advanced Research and Reviews 15, no. 3 (September 30, 2022): 290–97. http://dx.doi.org/10.30574/wjarr.2022.15.3.0919.
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One of the world’s main causes of cancer-related fatalities worldwide is colorectal cancer. The adherent epithelial cells known as HCT116 (human colorectal carcinoma) are frequently employed to examine inflammatory responses in colonic epithelial cells. They are derived from the human colorectal cancer cell line. Crocin, a potent antioxidant, anticarcinogenic was tested in this study to see how it affected the HCT-116 human colorectal cancer cell line. MTT analysis was used to assess cell viability. Crocin's antiproliferative activity to inhibit the proliferation of HCT 116 cancer cells was examined. Crocin displayed the outstanding activities for MTT test, IC50= 10.57 μL/mL for 24 hours was calculated as IC50= 3.29 μL/mL for 48 hours on HCT 116 cell line. Total antioxidant status (TAS) and total oxidant status (TOS) in the prepared cell lysate were determined by using commercial kits. Crocin is thought to be a high potential agent to be used in treatment.
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Adnan, Mohd, Arif Jamal Siddiqui, Walid Sabri Hamadou, Mejdi Snoussi, Riadh Badraoui, Syed Amir Ashraf, Arshad Jamal, et al. "Deciphering the Molecular Mechanism Responsible for Efficiently Inhibiting Metastasis of Human Non-Small Cell Lung and Colorectal Cancer Cells Targeting the Matrix Metalloproteinases by Selaginella repanda." Plants 10, no. 5 (May 14, 2021): 979. http://dx.doi.org/10.3390/plants10050979.
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Selaginella species are known to have antimicrobial, antioxidant, anti-inflammatory, anti-diabetic as well as anticancer effects. However, no study has examined the cytotoxic and anti-metastatic efficacy of Selaginella repanda (S. repanda) to date. Therefore, this study aimed to evaluate the potential anti-metastatic properties of ethanol crude extract of S. repanda in human non-small-cell lung (A-549) and colorectal cancer (HCT-116) cells with possible mechanisms. Effect of S. repanda crude extract on the growth, adhesion, migration and invasion of the A-549 and HCT-116 were investigated. We demonstrated that S. repanda crude extract inhibited cell growth of metastatic cells in a dose and time dependent manner. Incubation of A-549 and HCT-116 cells with 100–500 µg/mL of S. repanda crude extract significantly inhibited cell adhesion to gelatin coated surface. In the migration and invasion assay, S. repanda crude extract also significantly inhibited cellular migration and invasion in both A-549 and HCT-116 cells. Moreover, reverse transcription-polymerase chain reaction, and real-time PCR (RT-PCR) analysis revealed that the activity and mRNA level of matrix metalloproteinase-9 (MMP-9), matrix metalloproteinase-2 (MMP-2) and membrane type 1-matrix metalloproteinase (MT1-MMP) were inhibited. While the activity of tissue inhibitor matrix metalloproteinase 1 (TIMP-1); an inhibitor of MMPs was stimulated by S. repanda crude extract in a concentration-dependent manner. Therefore, the present study not only indicated the inhibition of motility and invasion of malignant cells by S. repanda, but also revealed that such effects were likely associated with the decrease in MMP-2/-9 expression of both A-549 and HCT-116 cells. This further suggests that S. repanda could be used as a potential source of anti-metastasis agent in pharmaceutical development for cancer therapy.
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Ciftci, Halilibrahim, Belgin Sever, Firdevs Ocak, Nilüfer Bayrak, Mahmut Yıldız, Hatice Yıldırım, Hasan DeMirci, et al. "In Vitro and In Silico Study of Analogs of Plant Product Plastoquinone to Be Effective in Colorectal Cancer Treatment." Molecules 27, no. 3 (January 21, 2022): 693. http://dx.doi.org/10.3390/molecules27030693.
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Plants have paved the way for the attainment of molecules with a wide-range of biological activities. However, plant products occasionally show low biological activities and/or poor pharmacokinetic properties. In that case, development of their derivatives as drugs from the plant world has been actively performed. As plant products, plastoquinones (PQs) have been of high importance in anticancer drug design and discovery; we have previously evaluated and reported the potential cytotoxic effects of a series of PQ analogs. Among these analogs, PQ2, PQ3 and PQ10 were selected for National Cancer Institute (NCI) for in vitro screening of anticancer activity against a wide range of cancer cell lines. The apparent superior anticancer potency of PQ2 on the HCT-116 colorectal cancer cell line than that of PQ3 and PQ10 compared to other tested cell lines has encouraged us to perform further mechanistic studies to enlighten the mode of anti-colorectal cancer action of PQ2. For this purpose, its apoptotic effects on the HCT-116 cell line, DNA binding capacity and several crucial pharmacokinetic properties were investigated. Initially, MTT assay was conducted for PQ2 at different concentrations against HCT-116 cells. Results indicated that PQ2 exhibited significant cytotoxicity in HCT-116 cells with an IC50 value of 4.97 ± 1.93 μM compared to cisplatin (IC50 = 26.65 ± 7.85 μM). Moreover, apoptotic effects of PQ2 on HCT-116 cells were investigated by the annexin V/ethidium homodimer III staining method and PQ2 significantly induced apoptosis in HCT-116 cells compared to cisplatin. Based on the potent DNA cleavage capacity of PQ2, molecular docking studies were conducted in the minor groove of the double helix of DNA and PQ2 presented a key hydrogen bonding through its methoxy moiety. Overall, both in vitro and in silico studies indicated that effective, orally bioavailable drug-like PQ2 attracted attention for colorectal cancer treatment. The most important point to emerge from this study is that appropriate derivatization of a plant product leads to unique biologically active compounds.
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Al Monla, Reem, Zeina Dassouki, Achraf Kouzayha, Yahya Salma, Hala Gali-Muhtasib, and Hiba Mawlawi. "The Cytotoxic and Apoptotic Effects of the Brown Algae Colpomenia sinuosa are Mediated by the Generation of Reactive Oxygen Species." Molecules 25, no. 8 (April 24, 2020): 1993. http://dx.doi.org/10.3390/molecules25081993.
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Brown algae are a novel resource of biogenic molecules, however few studies have been conducted in the Mediterranean to assess the cytotoxic mechanisms of algal-derived compounds. This study focuses on the antineoplastic activity of extracts from non-investigated algae of the Lebanese coast, Colpomenia sinuosa. Extracts’ antineoplastic activities were evaluated by MTT and trypan blue on different tumorigenic cells. Results indicated that the most potent extract was obtained by soxhlet using dichloromethane:methanol solvent (DM soxhlet) against HCT-116. Wound healing assay confirmed that this extract decreased the migration potential of HCT-116 cells with minimal effects on non-tumorigenic cells. It also induced an increase in the subG1 population as determined by flow cytometry. Western blot analysis demonstrated that apoptosis in treated HCT-116 cells was induced via upregulation of p21 protein and downregulation of the anti-apoptotic Bcl 2, which led to caspases activation. The latter, catalyzes the degradation of PARP-1, and thus suppresses cancer proliferation. Morphological alterations, further confirmed apoptosis. A strong pro-oxidant activity evidenced by the enhanced generation of reactive oxygen species (ROS) was observed in HCT-116 treated cells. Interestingly, a strong antioxidant effectively blocked effect induced by the extract. These results indicate that C. sinuosa is a source of bioactive compounds possessing pro-apoptotic and anti-migratory efficacy.
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Lee, Myeong-Seon, and Sung-Ho An. "Chemotherapeutic Response of Doxorubicin and Ascorbate in HCT-116 Cells." Joural of the Korea Entertainment Industry Association 5, no. 4 (December 31, 2011): 188. http://dx.doi.org/10.21184/jkeia.2011.12.5.4.188.
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Tsai, Cheng-Chih, Kuan-Jung Huang, and Pei-Pei Lin. "Lactobacillus spp. inhibits the growth of HCT-116 and reduces IL-8 secretion by Salmonella typhimurium-infected HCT-116 colorectal carcinoma cells." International Journal of Food Studies, no. 2 (October 18, 2022): 307–19. http://dx.doi.org/10.7455/ijfs/11.2.2022.a5.
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Salmonella typhimurium causes symptoms resembling typhoid fever and gastroenteritis in humans. Its toxicity is due to an outer membrane consisting largely of lipopolysaccharides (LPS) which is responsible for the host immune response. The aim of this study is to evaluate the antimicrobial, anti-apoptotic ability of Lactobacillus plantarum and reduce Salmonella-induced pro-inflammatory cytokine IL-8 secretion. Adhesive tests were performed using lactobacilli co-cultured with the colon cancer cell line HCT-116 for 2 hours. The strains displaying the highest adhesion were selected for downstream 3- (4, 5- Dimethylthiazol -2-yl) -2, 5- diphenyltetrazolium bromide (MTT) tests to assess cytotoxicity. The supernatants of Lactobacillus cultured with HCT-116 cells for 24 and 48 h to evaluate the inhibitory effect. To determine Interleukin 8 (IL-8) secretion in colon cancer induced by S. typhimurium, we stimulated HCT-116 cells with S. typhimurium and co-cultured with lactobacilli for 24 h. Lactobacilli had the most significant inhibitory effects on cell growth, and their inhibitory effects were time-dependent. Strain No. 03-03-026 caused cancer cell deoxyribonucleic acid (DNA) fragmentation, and the anti-apoptosis protein (B-cell lymphoma 2) was reduced in the HCT-116 cells as determined. IL-8 production in colon cancer cells was significantly reduced by these lactobacilli. Our results suggested that lactobacilli maybe effectively reduce the numbers of S. typhimurium, IL-8 levels and the anti-apoptotic phosphorylated-p38 mitogen-activated protein kinase and B-cell lymphoma 2 proteins. Lactobacillus can be added to the diet as a food additive to prevent colorectal cancer and used to be the prophylactic agent against S. typhimurium.
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Zelen, Ivanka, Milan Zarić, Petar P. Čanović, Danica Igrutinović, and Ana Rilak Simović. "Antitumor activity of ruthenium(II) complexes on HCT 116 cell line in vitro." Education and Research in Health Sciences 1, no. 1 (December 26, 2022): 6–12. http://dx.doi.org/10.5937/erhs2201006z.
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In the field of non-platinum complexes, ruthenium complexes have shown very strong antitumor activity on various types of cisplatin-resistant tumors. In addition, Ru(II) and Ru(III) complexes have shown a high degree of selectivity towards cancer cells as well as antimetastatic effects. Importantly, ruthenium compounds can bind to the DNA molecule of a tumor cell and thus reduce the viability of cancer cells. Moreover, ruthenium complexes can bind to human serum albumin and transferrin, which makes their transfer to tumor cells more efficient than platinum compounds. Consequently, the research aim was to investigate the antitumor effect of two synthesized Ru(II) complexes [Ru(Cl-Ph-tpy)(phen)Cl]Cl (K1) and [Ru(Cl-Ph-tpy)(o-bqdi)Cl]Cl (K2) on the HCT 116 cell line, and to define the mechanism of cell death that these compounds induce in HCT 116 cancer cells. Results of our research clearly showed that the two investigated ruthenium complexes K1 and K2 showed very strong antitumor activity against the HCT 116 tumor cell line. Additionally, ruthenium complex K1 showed higher antitumor activity than ruthenium K2 complex and cisplatin after 72 hours of treatment. Our findings demonstrated that both K1 and K2 ruthenium compounds exhibited strong antitumor activity against HCT 116 cell line by induction of early apoptosis.
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Shacham, S., M. Kauffman, V. Sandanayaka, G. Draetta, S. Shechter, J. Williams, and R. Nir. "Preclinical development of small-molecule CRM1 inhibitors as novel therapy for the treatment of colorectal cancer (CRC)." Journal of Clinical Oncology 29, no. 4_suppl (February 1, 2011): 430. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.430.
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430 Background: CRM1 (XPO1) is a key nuclear export protein which controls the location of multiple tumor suppressor (TSP) and growth regulatory (GRP) proteins including p53, PI3K/AKT, Wnt/ß-catenin and NF-kB. Forced nuclear expression of TSP and GRP by CRM1 inhibition can lead to apoptosis in cancer cells while sparing normal cells. Methods: Novel small-moleculeCRM1 inhibitors were synthesized and nuclear distribution studies were performed in cells transfected with HIV-rev GFP proteins. Cell proliferation studies were performed in 16 CRC cell lines: LS-123, SW-626, Colo-201, Colo-205, Colo-320DM, Colo-320HSR, Lovo, DLD-1, HCT-15, WiDi, LS-174T, LS-180, SW-620, C2BBe1, HCT-8, HCT-116, and in human peripheral leukocytes (PBMC). Cellular distribution and apoptosis assays were performed on HCT-116. Antitumor activity is assessed in human HCT-116 xenografts in scid-mice. Results: The lead CRM1 inhibitor, KPT-0127, blocks CRM1 mediated nuclear export of HIV-Rev-GFP, FOXO, and p53 with an IC50 of ∼300 nM. KPT-0127 is cytotoxic to various CRC cell lines with EC50s of 0.07-1.1 μM; in 9 CRC lines EC50s were < 0.3 mM. In contrast, normal cell lines and PBMCs had EC50 > 5-20 μM. In HCT- 116 cells, KPT-0127 induces cell cycle arrest at both G1/S and G2/M checkpoints and dose dependently increases nuclear p53, followed by an increase in caspase 3. KTP-0127 10μM shows no significant effect on 37 proteins including several cysteine proteases. In mice, KPT-0127 given by SC injection of 30-100 mg/kg leads to serum levels exceeding the effective CRM1 inhibitory concentration for at least 4 hours and is well tolerated. KPT-0127 given SC to mice bearing HCT-116 colon xenografts results in dose-dependent antitumor activity. Conclusions: The novel small- molecule CRM1 inhibitor KTP-0127 kills CRC lines with multiple TSP, GRP, and oncogenic abnormalities, including p53 mutations/deletions and PTEN deficiency/AKT activation, while sparing normal cells. This likely reflects the ability of CRM1 inhibition to affect multiple critical and non-redundant regulatory pathways. These results support the development of CRM1 inhibitors for the treatment of CRC. IND-enabling CMC and toxicology work are in preparation. [Table: see text]
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Mahajna, Shahinaz, Sleman Kadan, Zipora Tietel, Bashar Saad, Said Khasib, Aziz Tumeh, Doron Ginsberg, and Hilal Zaid. "In Vitro Evaluation of Chemically Analyzed Hypericum Triquetrifolium Extract Efficacy in Apoptosis Induction and Cell Cycle Arrest of the HCT-116 Colon Cancer Cell Line." Molecules 24, no. 22 (November 15, 2019): 4139. http://dx.doi.org/10.3390/molecules24224139.
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Naturally derived drugs and plant-based products are attractive commodities that are being explored for cancer treatment. This in vitro study aimed to investigate the role of Hypericum triquetrifolium (50% ethanol: 50% water) extract (HTE) treatment on apoptosis, cell cycle modulation, and cell cycle arrest in human colon cancer cell line (HCT-116). HTE induced cell death via an apoptotic process, as assayed by an Annexin V-Cy3 assay. Exposing HCT-116 cells to 0.064, 0.125, 0.25, and 0.5 mg/mL of HTE for 24 h led to 50 ± 9%, 71.6 ± 8%, 85 ± 5%, and 96 ± 1.5% apoptotic cells, respectively. HCT-116 cells treated with 0.25 and 0.5 mg/mL HTE for 3 h resulted in 38.9 ± 1.5% and 57.2 ± 3% cleavage of caspase-3-specific substrate, respectively. RT-PCR analysis revealed that the HTE extract had no effect on mRNA levels of Apaf-1 and NOXA. Moreover, the addition of 0.125 mg/mL and 0.25 mg/mL HTE for 24 h was clearly shown to attenuate the cell cycle progression machinery in HCT-116 cells. GC/MS analysis of the extract identified 21 phytochemicals that are known as apoptosis inducers and cell cycle arrest agents. All the compounds detected are novel in H. triquetrifolium. These results suggest that HTE-induced apoptosis of human colon cells is mediated primarily through the caspase-dependent pathway. Thus, HTE appears to be a potent therapeutic agent for colon cancer treatment.
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Lee, Ko-Chao, Kuen-Lin Wu, Shun-Fu Chang, Hsin-I. Chang, Cheng-Nan Chen, and Yih-Yuan Chen. "Fermented Ginger Extract in Natural Deep Eutectic Solvent Enhances Cytotoxicity by Inhibiting NF-κB Mediated CXC Chemokine Receptor 4 Expression in Oxaliplatin-Resistant Human Colorectal Cancer Cells." Antioxidants 11, no. 10 (October 19, 2022): 2057. http://dx.doi.org/10.3390/antiox11102057.
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Ginger extracts have been shown to have health-promoting pharmacological activity and beneficial effects, including antioxidant and anticancer properties. The extraction of ginger by natural deep eutectic solvents (NaDES) has been shown to enhance bioactivity, but the cytotoxicity of NaDES extracts needs to be further determined. Signaling through the CXC chemokine receptor 4 (CXCR4) expressed on colorectal cancer (CRC) cells has a pivotal role in tumor cell chemosensitivity. Oxaliplatin is a third-generation platinum compound used as an effective chemotherapeutic drug for CRC treatment. However, whether ginger extract and oxaliplatin could induce a synergistic cytotoxic effect in oxaliplatin-resistant CRC cells through modulating CXCR4 expression is not known. In this study, oxaliplatin-resistant HCT-116 (HCT-116/R) cells were generated first. Ginger was extracted using the NaDES mixture betaine/lactate/water (1:2:2.5). Lactobacillus reuteri fermentation of NaDES-ginger extract increased the total polyphenol content (12.42 mg gallic acid/g in non-fermented NaDES-ginger extract and 23.66 mg gallic acid/g in fermented NaDES-ginger extract). It also increased the antioxidant activity by about 20–30% compared to non-fermented NaDES-ginger extract. In addition, it achieved low cytotoxicity to normal colonic mucosal cells and enhanced the anticancer effect on HCT-116/R cells. On the other hand, the inhibition of NF-κB activation by fermented NaDES-ginger extract significantly decreased the CXCR4 expression (p < 0.05) in HCT-116/R cells. The inactivation of NF-κB by pharmacological inhibitor pyrrolidine dithiocarbamate further enhanced the fermented NaDES-ginger extract-reduced CXCR4 expression levels (p < 0.05). Moreover, fermented NaDES-ginger extract could synergistically increase the cytotoxicity of oxaliplatin by inhibiting CXCR4 expression and inactivating NF-κB, resulting in HCT-116/R cell death. These findings demonstrate that fermented NaDES-ginger extract reduces the NF-kB-mediated activation of CXCR4 and enhances oxaliplatin-induced cytotoxicity in oxaliplatin-resistant CRC cells.
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Fernández-Tomé, Samuel, Fei Xu, Yanhui Han, Blanca Hernández-Ledesma, and Hang Xiao. "Inhibitory Effects of Peptide Lunasin in Colorectal Cancer HCT-116 Cells and Their Tumorsphere-Derived Subpopulation." International Journal of Molecular Sciences 21, no. 2 (January 14, 2020): 537. http://dx.doi.org/10.3390/ijms21020537.
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The involvement of cancer stem-like cells (CSC) in the tumor pathogenesis has profound implications for cancer therapy and chemoprevention. Lunasin is a bioactive peptide from soybean and other vegetal sources with proven protective activities against cancer and other chronic diseases. The present study focused on the cytotoxic effect of peptide lunasin in colorectal cancer HCT-116 cells, both the bulk tumor and the CSC subpopulations. Lunasin inhibited the proliferation and the tumorsphere-forming capacity of HCT-116 cells. Flow cytometry results demonstrated that the inhibitory effects were related to apoptosis induction and cell cycle-arrest at G1 phase. Moreover, lunasin caused an increase in the sub-GO/G1 phase of bulk tumor cells, linked to the apoptotic events found. Immunoblotting analysis further showed that lunasin induced apoptosis through activation of caspase-3 and cleavage of PARP, and could modulate cell cycle progress through the cyclin-dependent kinase inhibitor p21. Together, these results provide new evidence on the chemopreventive activity of peptide lunasin on colorectal cancer by modulating both the parental and the tumorsphere-derived subsets of HCT-116 cells.
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Liu, Kuo-Ching, Ting-Ying Shih, Chao-Lin Kuo, Yi-Shih Ma, Jiun-Long Yang, Ping-Ping Wu, Yi-Ping Huang, Kuang-Chi Lai, and Jing-Gung Chung. "Sulforaphane Induces Cell Death Through G2/M Phase Arrest and Triggers Apoptosis in HCT 116 Human Colon Cancer Cells." American Journal of Chinese Medicine 44, no. 06 (January 2016): 1289–310. http://dx.doi.org/10.1142/s0192415x16500725.
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Sulforaphane (SFN), an isothiocyanate, exists exclusively in cruciferous vegetables, and has been shown to possess potent antitumor and chemopreventive activity. However, there is no available information that shows SFN affecting human colon cancer HCT 116 cells. In the present study, we found that SFN induced cell morphological changes, which were photographed by contrast-phase microscopy, and decreased viability. SFN also induced G2/M phase arrest and cell apoptosis in HCT 116 cells, which were measured with flow cytometric assays. Western blotting indicated that SFN increased Cyclin A, cdk 2, Cyclin B and WEE1, but decreased Cdc 25C, cdk1 protein expressions that led to G2/M phase arrest. Apoptotic cell death was also confirmed by Annexin V/PI and DAPI staining and DNA gel electrophoresis in HCT 116 cells after exposure to SFN. The flow cytometric assay also showed that SFN induced the generation of reactive oxygen species (ROS) and Ca[Formula: see text] and decreased mitochondria membrane potential and increased caspase-8, -9 and -3 activities in HCT 116 cell. Western blotting also showed that SFN induced the release of cytochrome c, and AIF, which was confirmed by confocal microscopy examination. SFN induced ER stress-associated protein expression. Based on those observations, we suggest that SFN may be used as a novel anticancer agent for the treatment of human colon cancer in the future.
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Лунёва, К. А., О. Е. Клементьева, К. Э. Терновская, Е. А. Дубова, and А. С. Лунёв. "Xenograft heterotopic modeling of colorectal cancer of various cell types in athymic BALB/c nude mice." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 4() (December 18, 2020): 148–52. http://dx.doi.org/10.25557/0031-2991.2020.04.148-152.
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Введение. Высокий уровень заболеваемости колоректальным раком стимулирует поиск методов его своевременной диагностики и эффективной терапии, что, в свою очередь, предполагает использование адекватных животных моделей на стадиях разработки и доклинических исследований. Методика. Для моделирования гетеротопических ксенографтов были использованы клеточные культуры колоректального рака человека линий DLD-1, HCT 116 и HT-29. В качестве носителей опухолевых моделей были взяты мыши линии BALB/c nude. Суспензию клеток вводили подкожно в область лопатки с помощью шприца. Результаты. Полученные из Американской коллекции типовых культур (ATCC) клетки культивировали до достижения необходимого количества для моделирования ксенографтов (20 сут). Клетки линии HCT-116 культивировались активнее и образовывали монослой в 3 раза быстрее, чем клетки линии DLD-1 и HT-29. Выживаемость мышей после проведения процедуры подкожной ксенотрансплантации составляла 100%. Образование ксенографтов объемом около 1 см3 наблюдали на 17-е - 26-е сут после прививания клеток. Приживаемость введённых клеток составила 100% для линии HCT-116. Для клеток колоректального рака человека линий DLD-1 и HT-29 приживаемость составила 75% и 60%, соответственно. Заключение. При экспериментальном моделировании подкожных гетеротопических ксенографтов колоректального рака человека на мышах линии BALB/c nude была получена высокая степень воспроизводимости при 100%-ной выживаемости животных-носителей. Introduction. The high prevalence of colorectal cancer (СС) stimulates scientists and physicians to search methods for СС diagnosis and effective therapy, which requires appropriate animal models at the stage of development and preclinical studies. Methods. CC cell cultures (DLD-1, HCT 116, and HT-29) were used for heterotopic xenograft modeling in BALB/c nude mice. The cell suspension was injected subcutaneously with a syringe. Results. CC cells from ATCC (American Type Culture Collection) were cultivated until obtaining the required number of cells for xenograft modeling (20 days). The HCT-116 cell culture developed more actively and formed a monolayer three times faster than DLD-1 and HT-29 cells. Survival of the mice after subcutaneous transplantation was 100%. Xenografts of approximately 1 cm3 volume formed at 17-26 days after grafting. Transplantability of the injected cells was 100% for HCT-116, 75% for DLD-1, and 60% for HT-29. Conclusion. The experimental modeling of subcutaneous heterotopic CC xenografts in BALB/c nude mice showed a high level of reproducibility with absolute 100% - survival of recipient mice.
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Mostafa, Yasser S., Saad A. Alamri, Mohammad Y. Alfaifi, Sulaiman A. Alrumman, Serag Eldin I. Elbehairi, Tarek H. Taha, and Mohamed Hashem. "L-Glutaminase Synthesis by Marine Halomonas meridiana Isolated from the Red Sea and Its Efficiency against Colorectal Cancer Cell Lines." Molecules 26, no. 7 (March 31, 2021): 1963. http://dx.doi.org/10.3390/molecules26071963.
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L-glutaminase is an important anticancer agent that is used extensively worldwide by depriving cancer cells of L-glutamine. The marine bacterium, Halomonas meridian was isolated from the Red Sea and selected as the more active L-glutaminase-producing bacteria. L-glutaminase fermentation was optimized at 36 h, pH 8.0, 37 °C, and 3.0% NaCl, using glucose at 1.5% and soybean meal at 2%. The purified enzyme showed a specific activity of 36.08 U/mg, and the molecular weight was found to be 57 kDa by the SDS-PAGE analysis. The enzyme was highly active at pH 8.0 and 37 °C. The kinetics’ parameters of Km and Vmax were 12.2 × 10−6 M and 121.95 μmol/mL/min, respectively, which reflects a higher affinity for its substrate. The anticancer efficiency of the enzyme showed significant toxic activity toward colorectal adenocarcinoma cells; LS 174 T (IC50 7.0 μg/mL) and HCT 116 (IC50 13.2 μg/mL). A higher incidence of cell death was observed with early apoptosis in HCT 116 than in LS 174 T, whereas late apoptosis was observed in LS 174 T more than in HCT 116. Also, the L-glutaminase induction nuclear fragmentation in HCT 116 was more than that in the LS 174T cells. This is the first report on Halomonas meridiana as an L-glutaminase producer that is used as an anti-colorectal cancer agent.
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Leuner, Olga, Jaroslav Havlik, Milos Budesinsky, Vladimir Vrkoslav, Jessica Chu, Tracey D. Bradshaw, Jana Hummelova, et al. "Cytotoxic Constituents of Pachyrhizus Tuberosus from Peruvian Amazon." Natural Product Communications 8, no. 10 (October 2013): 1934578X1300801. http://dx.doi.org/10.1177/1934578x1300801022.
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Investigations into the chemical constituents of the seeds of the neglected tuber crop Pachyrhizus tuberosus (Leguminosae) resulted in the isolation of seven components: five rotenoids [12a-hydroxyerosone (1), 12a-hydroxydolineone (2), erosone (3), 12a-hydroxyrotenone (4) and rotenone (6)], a phenylfuranocoumarin [pachyrrhizine (5)] and an isoflavanone [neotenone (7)]. The compounds were isolated using several chromatography techniques and characterized and verified by NMR and HPLC/MS. The MTT assay was used to examine the selective cytotoxic effects of the methanolic P. tuberosus extract and isolated compounds in two human cancer cell lines [breast (MCF-7) and colorectal (HCT-116)] and in non-transformed human fibroblasts (MRC-5); IC50 values were calculated. The methanolic P. tuberosus extract displayed respectable cytotoxic effects against HCT-116 and MCF-7 cells with IC50 values of 7.3 and 6.3 μg/mL, respectively. Of the compounds, 6 exacted greatest cytotoxicity and selectivity towards the cancer cell lines tested, yielding IC50 values of 0.3 μg/mL against both MCF-7 and HCT-116 cells, and a 6-fold reduced activity against MRC-5 fibroblasts. Compound 4 also demonstrated cytotoxicity against MCF-7 and HCT-116 (1.1 and 1.8 μg/mL, respectively), and reduced cytotoxicity towards MRC-5 cells (7.5 μg/mL). The results revealed from the in vitro cytotoxic MTT assay are worthy of further antitumor investigation.
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Tan, Maria Carmens, Glenn G. Oyong, Chien Chang Shen, and Consolacion Y. Ragasa. "CYTOTOXIC LABDANE DITERPENOIDS FROM ANDROGRAPHIS PANICULATA (BURM.F.) NEES." Asian Journal of Pharmaceutical and Clinical Research 10, no. 12 (December 1, 2017): 99. http://dx.doi.org/10.22159/ajpcr.2017.v10i12.19194.
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Objective: The primary objective of this study was to probe the cytotoxic capacity of the labdane diterpenoids andrographolide (1), 14-deoxyandrographolide (2), 14-deoxy-12-hydroxyandrographolide (3), and neoandrographolide (4) on mutant and wild-type immortalized cell lines.Methods: Breast adenocarcinoma (MCF-7), colon carcinomas (HCT-116 and HT-29), small cell lung carcinoma (H69PR), human acute monocytic leukemia (THP-1), and wild-type primary normal human dermal fibroblasts - neonatal cells (HDFn) were incubated with 1-4, and the degree of cytotoxicity was analyzed by employing the in vitro PrestoBlue® cell viability assay. Working solutions of 1-4 were prepared in complete cell culture medium to a final non-toxic dimethyl sulfoxide concentration of 0.2%. The plates were incubated at 37°C with 5% CO2 in a 98% humidified incubator throughout the assay. Nonlinear regression and statistical analyses were done to extrapolate the half maximal inhibitory concentration 50% (IC50). One-way ANOVA (p<0.05) and multiple comparison, Tukey’s post hoc test (p<0.05), were used to compare different pairs of data sets. Results were considered statistically significant at p<0.05.Results: The highest cytotoxicity index was exhibited by the H69PR and 1 trials which displayed the lowest IC50 value of 3.66 μg/mL, followed by HT-29 treated with 2, HCT-116 and 1 trials, and H69PR treated with 4 (IC50=3.81, 3.82, and 4.19 μg/mL, respectively). Only 1 and 4 were detrimental toward MCF-7, while 1, 3, and 4 were degenerative against H69PR. Tukey’s post hoc multiple comparison indicated no significant difference in the cytotoxicity of 1-4 on HCT-116 cells which afforded IC50 values ranging from 3.82 to 5.12 μg/mL. Evaluation of the two colon carcinoma cell lines showed that HCT-116 was categorically more susceptible to cellular damage caused by treatments with 1-4 than was HT-29. Cytotoxicity was not detected in THP-1 and HDFn cells (IC50>100 μg/mL).Conclusion: Diterpenoids 1-4 isolated from the dichloromethane extract of the leaves of A. paniculata exhibited different cytotoxic activities against MCF-7, HCT-116, HT-29, and H69PR. All constituents had comparable action on HCT-116 cells but were not found to be cytotoxic to normal HDFn cells and mutant THP-1 cells.
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Vaziri, S. A., A. Al-Hazzouri, D. R. Grabowski, M. K. Ganapathi, R. M. Bukowski, and R. Ganapathi. "Sorafenib treatment of clear-cell renal cell carcinoma (CCRCC) and colorectal carcinoma (CRC) cells: Differential effects on gene expression and cell death pathways." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 15612. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.15612.
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15612 Background: The von Hippel Lindau gene (VHL) is often mutated in CCRCC and leads to loss of VHL protein (pVHL) expression. Sorafenib is a TKI with clinical activity in metastatic CCRCC. Studies to define mechanisms governing anti-tumor activity of this agent in CCRCC or CRC cell lines that express wild-type pVHL were conducted. Methods: We evaluated CAKI-1 (CCRCC) and HCT- 116/p53 +/+ (CRC) cell lines as model systems expressing wild-type pVHL. Cells were treated at 37°C in an atmosphere of normoxia (21% O2) or hypoxia (1% O2), 5% CO2 and the remainder N2 in the absence (control) or presence of sorafenib (2.5–20 μM) for 24–96 hours. Expression of target angiogenesis, apoptotic and anti-apoptotic genes was determined by real-time RT- PCR. Fluorescence microscopy following staining with Hoechst 33342 plus propidium iodide was used to analyze cell death by apoptosis and/or necrosis. Caspase-3 activity was measured using the target substrate DEVD-AFC. Results: In CAKI-1 and HCT-116 cells, exposure to 1% O2 relative to 21% O2, led to increased expression (2 to 6-fold) of angiogenesis (VEGF) and anti-apoptosis (TNFAIP3 & MCF2) genes. However, in an atmosphere of 1% O2 relative to 21% O2, a decreased (>2-fold) and increased (>3-fold) expression of the apoptotic (TNFRSF25) gene was observed in CAKI-1 cells and HCT-116 cells. Sorafenib treatment (7.5 μM) of CAKI-1 cells in 1% O2 led to a >3–4-fold decrease in expression of the VEGF and TNFAIP3 and a 3-fold increase TNFRSF25 genes. Following treatment with 10 μM sorafenib for 48h, cell death was >80% by necrosis in CAKI-1 cells and >95% by apoptosis in HCT-116 cells. Apoptotic cell death in the HCT-116 was also confirmed by increased caspase-3 activity in cell extracts following sorafenib treatment. Apoptotic cell death or necrotic cell death induced by sorafenib was unaffected by normoxia or hypoxia. Conclusions: In contrast to CCRCC cells, hypoxia led to upregulation of the apoptotic gene TNFRSF25 in the CRC cells. Anti- proliferative effects of sorafenib were primarily by necrosis in CCRCC cells and by apoptosis in CRC cells. No significant financial relationships to disclose.
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Lin, Beibei, Xuegu Xu, Xiaobi Zhang, Yinfei Yu, and Xiaoling Wang. "Photodynamic Treatment of Colorectal Cancer Using Chlorin e6-Loaded Poly(lactide-co-glycolide)- Based Nanoparticles." Journal of Biomedical Nanotechnology 17, no. 10 (October 1, 2021): 1939–50. http://dx.doi.org/10.1166/jbn.2021.3170.
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We prepared poly(lactide-co-glycolide) (PLGA) encapsulated with chlorin e6 (Ce6) in an effort to increase the stability and efficiency of photosensitizers for photodynamic therapy (PDT). We determined that Ce6-loaded PLGA nanoparticles (PLGA-Ce6 NPs) had drug-loading efficiency of 5%. The efficiency of encapsulation was 82%, the zeta potential was- 25 mV, and the average diameter was 130 nm. The encapsulation of Ce6 in PLGA nanoparticles showed excellent stability. The nanoparticles exhibited sustained Ce6 release profiles with 50% released at the end of 3 days, whereas free Ce6 showed rapid release within 1 day. Ce6 release patterns were controlled by encapsulation into PLGA. The uptake of PLGA-Ce6 NPs was significantly enhanced by endocytosis in the first 8 hours in the HCT-116 cell line. An intracellular reactive oxygen species assay revealed the enhanced uptake of the nanoparticles. An in vitro anti-tumor activity assay showed that the PLGA-Ce6 NPs exhibited enhanced phototoxicity toward HCT-116 cells and a slightly lower IC50 value in HCT-116 cells than Ce6 solution alone. Exposure of HCT-116 cell spheroids to PLGA-Ce6 NPs penetrated more profoundly and had better phototoxicity than pure drugs. These findings suggest that PLGA-Ce6 NPs might serve as PDT for colorectal cancer.
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Mahmoud, Alaa, Dana Elkhalifa, Feras Alali, Ala-Eddin Al Moustafa, and Ashraf Khalil. "Novel Polymethoxylated Chalcones as Potential Compounds Against KRAS-Mutant Colorectal Cancers." Current Pharmaceutical Design 26, no. 14 (May 15, 2020): 1622–33. http://dx.doi.org/10.2174/1381612826666200206095400.
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Background/Objective: KRAS-mutant colorectal cancers (CRC) are tumors that are associated with poor prognosis. However, no effective treatments are available to target them. Therefore, we designed and synthesized novel chalcone analogs, small organic molecules, to investigate their effects on KRAS-mutant CRC cells. Methods: Fourteen new chalcone analogs were synthesized, optimized, characterized, and tested against two KRAS-mutant CRC cell lines (HCT-116 and LoVo), one p-53 and BRAF mutant CRC cell line (HT-29) and one normal immortalized colon cells (NCE-1 E6/E7). Effects on cell viability, apoptosis, cell cycle, migration, colony formation, EMT, and angiogenesis were investigated. Results: Compounds 3 and 14 were the most effective. Compound 3 showed potent activity against HCT-116 and LoVo cell lines (GI50 of 6.10 μM and 7.00 μM, respectively). While compound 14 showed GI50 of 8.60 μM and 8.80 μM on HCT-116 and LoVo cell lines, respectively. Both compounds were approximately 2-3 times more selective toward cancer cells rather than normal colon cells. Compound 3 was effective in inducing apoptosis in HCT-116 cells via Bax upregulation and Bcl-2 downregulation. Invasion and metastasis of KRAS-mutant cells were modulated by compounds 3 and 14 through significant inhibition of cell migration and the prevention of colony formation. In addition, they reversed EMT by downregulation of EMT markers (vimentin, fascin, and β- catenin) and upregulation of cell-cell adhesion marker, E-cadherin. Furthermore, compounds 3 and 14 had significantly inhibited angiogenesis in ovo. Conclusion: Compounds 3 and 14 represent potent and selective leads for KRAS-mutant CRC cells, thus, further in vitro and in vivo studies are necessary to confirm their effect on KRAS-mutant CRCs.
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Hussein, Mohammed A., Mohamed M. Salah El-Din, Esraa M. Saleh, Ahmed T. Mostafa, Mahmoud T. Abd-Elazziz, Omnia M. Abdelrahman, Ahmed S. Mahmoud, Ahmed M. Moro, Ebtsam A. Abdel-Wahab, and Ali A. Ali. "Sildenafil (VIAGRATM): A Promising Anticancer Drug Against Certain Human Cancer Cell Lines." Asian Journal of Chemistry 33, no. 6 (2021): 1420–24. http://dx.doi.org/10.14233/ajchem.2021.23199.
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Sildenafil has been identified as the first agent for treating male erectile dysfunction and is a selective inhibitor of phosphodiesterase 5 (PDE5). Its chemical structure consists of three moieties named; 1-methyl-3-propyl-1H-pyrazolo[4,3-d]pyrimidin-7(6H)-one, 5-(2-ethoxy-1-ylsulfonyl)phenyl and 4-methylpiperazine. Many articles are reported the cytotoxic activity of each moiety individually. The combination into a single molecule (sildenafil) of these three structural features could have promising anti-cancer and cytotoxic effects. The study evaluated sildenafil cytototoxic activity in vitro against mammalian cell lines: MCF-7, HCT-116, HeLa cells and A-549 cells with their IC50 values. Sildenafil showed considerable cytotoxic activity (IC50 = 28.2 ± 0.92, 45.2 ± 1.5, 30.5 ± 0.87 and 60.5 ± 3.2 μg/mL) against HCT-116, MCF-7, A-549 and HeLa cells, respectively. HCT-116 was the most sensitive cell line towards sildenafil followed by A-549, A375, MCF-7 and HeLa cells. These findings shed light on the antitumor activity of sildenafil and its possible impact on potentiating of cytokines, antitumor and anti-inflammatory markers in tumour cells. These effects might be related to the structure feature of sildenafil.
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Mirnajafizadeh, Fatemeh, Deborah Ramsey, Shelli McAlpine, Fan Wang, and John Stride. "Nanoparticles for Bioapplications: Study of the Cytotoxicity of Water Dispersible CdSe(S) and CdSe(S)/ZnO Quantum Dots." Nanomaterials 9, no. 3 (March 20, 2019): 465. http://dx.doi.org/10.3390/nano9030465.
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Semiconductor nanocrystals or quantum dots (QDs) have unique optical and physical properties that make them potential imaging tools in biological and medical applications. However, concerns over the aqueous dispersivity, toxicity to cells, and stability in biological environments may limit the use of QDs in such applications. Here, we report an investigation into the cytotoxicity of aqueously dispersed CdSe(S) and CdSe(S)/ZnO core/shell QDs in the presence of human colorectal carcinoma cells (HCT-116) and a human skin fibroblast cell line (WS1). The cytotoxicity of the precursor solutions used in the synthesis of the CdSe(S) QDs was also determined in the presence of HCT-116 cells. CdSe(S) QDs were found to have a low toxicity at concentrations up to 100 µg/mL, with a decreased cell viability at higher concentrations, indicating a highly dose-dependent response. Meanwhile, CdSe(S)/ZnO core/shell QDs exhibited lower toxicity than uncoated QDs at higher concentrations. Confocal microscopy images of HCT-116 cells after incubation with CdSe(S) and CdSe(S)/ZnO QDs showed that the cells were stable in aqueous concentrations of 100 µg of QDs per mL, with no sign of cell necrosis, confirming the cytotoxicity data.
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Nurashikin Nordin, Anis, Irmanisha Ibrahim, Ahmad Fairuzabadi Mohd Mansor, Yumi Zuhanis Has-Yun Hashim, and Ioana Voiculescu. "Content Cytotoxicity Studies of Colorectal Carcinoma Cells Using Printed Impedance Sensors." Bulletin of Electrical Engineering and Informatics 6, no. 4 (December 1, 2017): 317–26. http://dx.doi.org/10.11591/eei.v6i4.851.
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Monitoring the effectiveness of drugs on cancer cells is crucial for chemotherapeutics studies. In-vitro cell-based biosensors can be used as an alternative for characteristic studies of cells’ response to drugs. Cell-based sensors provide real-time measurements and require smaller sample volumes compared to conventional T-flask measurement methods. This paper presents a biosensor that detects in real-time, impedance variations of human colon cancer, HCT-116 cells when treated with anti-cancer agent, 5-Fluorouracil (5-FU). Two different extracellular matrix (ECM); polyaniline and gelatin were tested and evaluated in terms of attachment quality. Polyaniline was found to provide the best attachment for HCT-116 cells and was used for cytotoxicity studies. Cytokinetic behavior indicated that 5-FU inhibited HCT-116 cells at IC50 of 6.8 µg/mL. Trypan blue exclusion method for testing cell viability was used to validate the impedance measurements, where the cancer cell concentrations were reduced to ~35% when treated with 2.5 µg/mL, and 50% when treated with 6.8 µg/mL. The results generated by the microfabricated impedance biosensor are comparable to the Trypan blue method since both gave similar cell growth trend. It can be concluded that the impedance biosensor has potential to be used as an alternative method in drug testing applications.
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Bukowski, Karol, Beata Marciniak, Mateusz Kciuk, Mariusz Mojzych, and Renata Kontek. "Pyrazolo[4,3-e]tetrazolo[1,5-b][1,2,4]triazine Sulfonamides as Novel Potential Anticancer Agents: Cytotoxic and Genotoxic Activities In Vitro." Molecules 27, no. 12 (June 11, 2022): 3761. http://dx.doi.org/10.3390/molecules27123761.
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In this paper, we present for the first time the evaluation of cytotoxicity and genotoxicity of de novo synthesized pyrazolo[4,3-e]tetrazolo[1,5-b][1,2,4]triazine sulfonamides MM129, MM130, and MM131 in human tumor cell lines: HeLa, HCT 116, PC-3, and BxPC-3. Cytotoxic and genotoxic properties of the tested compounds were estimated using the MTT assay, comet assay (alkaline and neutral version), and γ-H2AX immuno-staining. Examined sulfonamides exhibited strong anticancer properties towards tested cells in a very low concentration range (IC50 = 0.17–1.15 μM) after 72 h exposure time. The results of the alkaline and neutral version of the comet assay following 24 h incubation of the cells with tested compounds demonstrated the capability of heterocycles to induce significant DNA damage in exposed cells. HCT 116 cells were the most sensitive to the genotoxic activity of novel tricyclic pyrazolo[4,3-e]tetrazolo[1,5-b][1,2,4]triazine sulfonamides in the neutral version of the comet assay. Immunocytochemical detection of γ-H2AX showed an increase in DNA DSBs level in the HCT 116 cell line, after 24 h incubation with all tested compounds, confirming the results obtained in the neutral comet assay. Among all investigated compounds, MM131 showed the strongest cytotoxic and genotoxic activity toward all tested cell types. In conclusion, our results suggest that MM129, MM130, and MM131 exhibit high cytotoxic and genotoxic potential in vitro, especially towards the colorectal cancer cell line HCT 116. However, further investigations and analyses are required for their future implementation in the field of medicine.
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Karabay, Arzu, Asli Koc, Tulin Ozkan, Yalda Hekmatshoar, Asuman Sunguroglu, Fugen Aktan, and Zeliha Buyukbingol. "Methylsulfonylmethane Induces p53 Independent Apoptosis in HCT-116 Colon Cancer Cells." International Journal of Molecular Sciences 17, no. 7 (July 15, 2016): 1123. http://dx.doi.org/10.3390/ijms17071123.
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Liu, Tong, Jing-wen Yang, and Qing-huai Zhang. "Autophagy facilitates anticancer effect of 5-fluorouracil in HCT-116 cells." Journal of Cancer Research and Therapeutics 14, no. 7 (2018): 1141. http://dx.doi.org/10.4103/0973-1482.204898.
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Smith, Abigail F., and George Loo. "Upregulation of haeme oxygenase-1 by zinc in HCT-116 cells." Free Radical Research 46, no. 9 (June 8, 2012): 1099–107. http://dx.doi.org/10.3109/10715762.2012.690872.
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Smith, Abigail F., Jennifer Longpre, and George Loo. "Inhibition by zinc of deoxycholate-induced apoptosis in HCT-116 cells." Journal of Cellular Biochemistry 113, no. 2 (January 5, 2012): 650–57. http://dx.doi.org/10.1002/jcb.23394.
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Longpre, Jennifer, and George Loo. "Inhibition of deoxycholate-induced apoptosis in iron-depleted HCT-116 cells." Apoptosis 17, no. 1 (September 22, 2011): 70–78. http://dx.doi.org/10.1007/s10495-011-0655-4.
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Malyarenko, Olesya S., Tatiana I. Imbs, and Svetlana P. Ermakova. "In Vitro Anticancer and Radiosensitizing Activities of Phlorethols from the Brown Alga Costaria costata." Molecules 25, no. 14 (July 14, 2020): 3208. http://dx.doi.org/10.3390/molecules25143208.
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The anticancer and radiosensitizing effects of high-molecular-weight phlorethols CcPh (Mw = 2520 Da) isolated from the brown algae of Costaria costata on human colorectal carcinoma HCT 116 and HT-29 cells were investigated. Phlorethols CcPh possessed cytotoxic activity against HT-29 (IC50 = 92 μg/mL) and HCT 116 (IC50 = 94 μg/mL) cells. CcPh at non-toxic concentrations inhibited the colony formation in colon cancer cells and significantly enhanced their sensitivity to low non-toxic X-ray irradiation. The combinatory effect of radiation and CcPh was synergistic (Combination index < 0.7). Algal phlorethols might be prospective candidates as radiosensitizers to improve the scheme of radiotherapy.
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Singh, Mahendra Pal, Ki Hun Park, Tejinder Pal Khaket, and Sun Chul Kang. "CJK-7, a Novel Flavonoid from Paulownia tomentosa Triggers Cell Death Cascades in HCT-116 Human Colon Carcinoma Cells via Redox Signaling." Anti-Cancer Agents in Medicinal Chemistry 18, no. 3 (June 4, 2018): 428–37. http://dx.doi.org/10.2174/1871520617666171026170009.
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Background: Colon cancer is the second most common cancer to cause death worldwide. About half of colon cancers patients require adjuvant therapy to control relapse following surgical resection. Therefore, abolition of tumor cell progression using an effective chemotherapeutic agent holds a feasible approach to treat patients suffering from colon cancer. In the present study, we evaluated the effects of geranylated flavonoid CJK-7, isolated from Paulownia tomentosa on HCT-116 human colon carcinoma cells. Materials and Methods: The effects of CJK-7 as an active component on HCT-116 cells programmed cell death and its underlying molecular mechanism were examined by using MTT assay, morphological assessment, H2DCFDA staining, Fura-2AM staining, Hoechst-33342 staining, comet assay, Acridine orange staining, mitochondrial membrane potential (ΔΨm) assay and Western blot analyses. Results and Conclusion: The results revealed that, CJK-7 was capable of inducing caspase-dependent cell death events in cancer cells. Moreover, it was involved in up-regulation of autophagy signaling as evidenced by enhanced expression of LC3I/II. We also noticed stimulated expression of endoplasmic reticulum stress markers and phosphorylation of c-Jun NH2-terminal kinase (JNK), which was associated with up-regulated expression of p53, PUMA, Atg5 and Beclin-1, and down-regulation of Bcl-2, stressing the interaction of ROS on the aforementioned signaling. Furthermore, exposure to ROS scavengers (N-acetyl-l-cysteine (NAC), and JNK-specific inhibitor SP600125) significantly reversed the effects of CJK-7 by down-regulating apoptosis and autophagy signatures in HCT-116 cancer cells. Collectively our findings clarify the ROS-dependent regulatory effect of CJK-7 on programmed cell death signaling events in HCT-116 cancer cells while depicting its virile pro-oxidant capacity.
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Bae, Inho, Taeyu Grace Kim, Taeyeon Kim, Dohoon Kim, Doug-Hoon Kim, Jaewon Jo, Young-Ju Lee, and Young-Il Jeong. "Phenethyl Isothiocyanate-Conjugated Chitosan Oligosaccharide Nanophotosensitizers for Photodynamic Treatment of Human Cancer Cells." International Journal of Molecular Sciences 23, no. 22 (November 9, 2022): 13802. http://dx.doi.org/10.3390/ijms232213802.
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The aim of this study is to synthesize phenethyl-conjugated chitosan oligosaccharide (COS) (abbreviated as ChitoPEITC) conjugates and then fabricate chlorin E6 (Ce6)-incorporated nanophotosensitizers for photodynamic therapy (PDT) of HCT-116 colon carcinoma cells. PEITC was conjugated with the amine group of COS. Ce6-incorporated nanophotosensitizers using ChitoPEITC (ChitoPEITC nanophotosensitizers) were fabricated by dialysis method. 1H nuclear magnetic resonance (NMR) spectra showed that specific peaks of COS and PEITC were observed at ChitoPEITC conjugates. Transmission electron microscope (TEM) confirmed that ChitoPEITC nanophotosensitizers have spherical shapes with small hydrodynamic diameters less than 200 nm. The higher PEITC contents in the ChitoPEITC copolymer resulted in a slower release rate of Ce6 from nanophotosensitizers. Furthermore, the higher Ce6 contents resulted in a slower release rate of Ce6. In cell culture study, ChitoPEITC nanophotosensitizers showed low toxicity against normal CCD986Sk human skin fibroblast cells and HCT-116 human colon carcinoma cells in the absence of light irradiation. ChitoPEITC nanophotosensitizers showed a significantly higher Ce6 uptake ratio than that of free Ce6. Under light irradiation, cellular reactive oxygen species (ROS) production of nanophotosensitizers was significantly higher than that of free Ce6. Especially, PEITC and/or ChitoPEITC themselves contributed to the production of cellular ROS regardless of light irradiation. ChitoPEITC nanophotosensitizers showed significantly higher PDT efficacy against HCT-116 cells than that of free Ce6. These results indicate that ChitoPEITC nanophotosensitizers have superior potential in Ce6 uptake, ROS production and PDT efficacy. In the HCT-116 cell-bearing mice tumor-xenograft model, ChitoPEITC nanophotosensitizers efficiently inhibited growth of tumor volume rather than free Ce6. In the animal imaging study, ChitoPEITC nanophotosensitizers were concentrated in the tumor tissue, i.e., fluorescence intensity in the tumor tissue was stronger than that of other tissues. We suggest that ChitoPEITC nanophotosensitizers are a promising candidate for the treatment of human colon cancer cells.
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Duangkaew, Methawee, and Wanatchaporn Arunmanee. "In vitro Screening for Cytotoxic Effect of Pore Forming Colicin N and Its Domains on Human Cancer Cells." Tropical Life Sciences Research 33, no. 1 (March 31, 2022): 163–77. http://dx.doi.org/10.21315/tlsr2022.33.1.10.
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Protein-based drugs have increasingly become an important segment of cancer treatment. In comparison with chemotherapy, they offer high efficacy and fewer side effects due to specifically targeting only cancer cells. Monoclonal antibodies are currently the main protein-based drugs in the market but their complexity and limitations in tumour penetration led to the development of alternative protein therapeutics such as pore-forming toxins. Colicin N (ColN), a pore-forming protein produced by E. coli, was previously found to exhibit cytotoxicity and selectivity in human lung cancer cells with promising potential for further development. Here we aimed to screen for the cytotoxicity of ColN in breast (MCF-7 and MDA-MB-231), lung (A549) and colon cancer cells (HT-29 and HCT-116) by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assay with various concentrations for 72 h and to investigate the cytotoxic effect of ColN domains on cancer cells. It showed that ColN mildly mediated the decrease in cell viability except for MCF-7. The highest effect was seen in A549 and HCT-116 cells which showed 31.9% and 31.5% decrease in cell viability, respectively. The mild inhibition or promotion of cancer cell proliferation by ColN tend to be based on the cell types. Furthermore, to search for the functional domain of ColN used for cytotoxicity, full-length ColN and truncated ColN with deletion of translocating, receptor binding and pore-forming domains were also tested on HCT-116 colon cancer cells. The findings indicated that HCT-116 cells were not significantly sensitive to ColN but full length ColN caused slight decrease in cancer cell viability. The data in this study will benefit the further development of ColN for alternative protein-based cancer therapy.