Relevant bibliographies by topics / HCT-116 cells

Academic literature on the topic 'HCT-116 cells'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "HCT-116 cells"

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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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Dissertations / Theses on the topic "HCT-116 cells"

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Perwaiz, Sunela. "Effect of 5-Flourouracil On HCT-116 P53+/- Human Colon Cancer Cells." Thesis, Högskolan i Skövde, Institutionen för vård och natur, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-6351.

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The purpose of this study was to observe the effects of 5-flourouracil on HCT-116 p53 +/- colon cancer cells. In order to investigate the effects of the drug, concentration-dependent assays and time-dependent  assay  procedures  were  used.  To  evaluate  the  cell  viability  after  being  treated with  the  drug,  XTT  technique  was  used.  After  performing  concentration-dependent  assays  a consequent  decrease  in  cell  viability  was  observed  with  increase  in  concentration  of  the  drug. The time-dependent assay showed a gradual decrease in cell viability with increase in time after exposure to the drug. Western blotting technique was performed on the proteins extracted from the samples. Expression of Bak was examined after the cells were exposed to the drug. Results from western blotting technique revealed that Bak protein was initially over-expressed after the cells were treated with 5-Flourouracil for 48 hours and this over-expression of the Bak resulted in   apoptosis   of   cancer   cells.   Thus,   5-Flourouracil   is   considered   to   be   an   effective chemotherapeutic  drug  for  colon  cancer  cells  partially  though  the  over-expression  of  Bak protein.
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Alotaibi, Moureq. "CELL DEATH AND GROWTH ARREST PATHWAYS MEDIATING THE ACTIONS OF STILBENE 5C IN HCT-116 COLON CANCER CELLS." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2851.

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Abstract The stilbene derivative, cis-3, 4’, 5-trimethoxy-3’-aminostilbene (stilbene 5c), is a potentially potent antitumor agent that acts via binding to the colchicine-binding pocket in microtubules. Earlier studies have shown that stilbene 5c induces cell death in ovarian cancer cells and leukemic cells. The present study was designed to investigate the effectiveness of this microtubule poison against the HCT-116 human colon cancer cell line and its mechanisms of action. Time course studies demonstrated that stilbene 5c produces a biphasic decrease in cell viability. The capacity of the cells to proliferate was not restored upon removal of the drug after 6 days of exposure. Consistent with the results of the time course studies, β-galactosidase staining indicated that treatment with stilbene 5c also promotes senescence. In addition to senescence, stilbene 5c-treated HCT-116 cells displayed formation of autophagic vesicles by acridine orange staining, which was supported by fluorescence-activated cell sorting (FACS). Further evidence of autophagy was derived from treatment of HCT116 cells carrying an RFP-LC3 construct with stilbene 5c, in which LC3 puncta formation increased in a time-dependent manner. DAPI staining, TUNEL, and Annexin 5 staining indicated that apoptosis is also occurring in stilbene 5c-treated HCT-116 cells. Cell cycle analysis demonstrated growth arrest at both G1 and G2/M, and an increase in the subG1 population at days 3 and 5, which correspond to senescence and apoptosis respectively. Interestingly, DAPI and Hoechst staining revealed morphological changes in the cell nuclei (binucleated and micronucleated cells), which suggest that mitotic catastrophe may also serve as a mode of cell death after treatment with stilbene 5c. However, our studies indicated that stilbene 5c works in a p53-independent manner. Exposure of P53-null HCT116 cells to stilbene resulted in a similar sensitivity as in p53-wild type HCT116 cells. We found that autophagic vacuoles were formed in response to stilbene 5c in p53-null HCT116 cells as well. Consistent with previous studies in other experimental cancer models, this work indicates that stilbene 5c could potentially be effective against colon cancer through the promotion of multiple modes of cell death.
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Gentile, Michelle Sara. "Analysis of p53 loss using combined metabolite and transcript profiling in HCT-116 colon cancer cells." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611322.

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Shipley, Lindsey C. BS, Harika MD Balagoni, Janet Lightner, Victoria PhD Palau, and Koyamangalath MD Krishnan. "15 Lox 1 Up-regulation and Cytotoxicity with γ-tocotrienol in HCT-116 Colon Cancer Cells." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/154.

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Colorectal cancer is the second leading cause of cancer-related deaths in the United States and the third most common cancer in men and women. Vitamin E is a lipid soluble antioxidant that exists as eight structurally different isoforms of tocopherols and tocotrienols. Recent experimental, and molecular studies suggest that γ-tocotrienol (GT3) may be a more potent cancer-preventive form of vitamin E. 15-lipoxygenase-1 (15-LOX-1) and its product 13-S-hydroxyoctadecadienoic acid (13-S-HODE) are decreased in colon cancer cells. 15 LOX-1 is considered a tumor suppressor gene in colon carcinogenesis. Non-steroidal anti-inflammatory drug (NSAID)-induced 15-LOX-1 expression is critical to aspirin and NSAID-induced apoptosis in colorectal cancer cells. HCT-116 is a microsatellite-instability (MSI) colon cancer cell line. MSI is a marker of chemo-resistance but is associated with improved survival as compared to microsatellite-stable (MSS) colon cancers. The effects of GT3 on cytotoxicity and 15 LOX-1 expression was studied on the human colon cancer cell line HCT-116. HCT-116 colon cancer cell lines were cultured in DMEM media and dosed with increasing concentrations of GT3 (20µM-50µM). Cytotoxicity of the drugs was studied using Cell Titer Glo and MTS assays 24 hours after dosing. Cells were then plated in 6-well plates and grown for 24 hours. Cells were then dosed with 2 mL of GT3 at 20 uM at the respective time periods (2h, 4h, 6h, 12h, 16h, 24h) and lysates were harvested. Gel electrophoresis was run according to BCA protein assay from the time-dependent lysates and blots were tagged with a rabbit 15-lox antibody. Ongoing experiments include RNA PCR. RNA is being isolated at 2, 4, 6 and 12 hours. The RNA as reversed transcribed using a 15 lox 1 primer and that cDNA is being quantified using Quantitative PCR. GT3 induced cytotoxicity in MTS assay and Cell Titer Glo assay when added to HCT-116 cell line. 15 LOX 1 protein expression was found to be up-regulated in the colon cancer cell line HCT-116 when GT3 was added at 12h, 16h and 24h with the maximum expression at 16 hours. Chemotherapeutic drugs can have significant side effects. Understanding the role of GT3 on colon cancer cell lines could lead to the development of novel drugs to supplement current chemotherapy regimens and allow for lower doses of chemotherapeutic agents. Modulation of 15-LOX-1 suggests that GT3 may induce apoptosis through induction of the lipoxygenase pathway. Further experiments are under way to study the mechanism of action of GT3 on the 15 LOX-1 pathway. Since HCT-116 is a MSI- colon cancer cell line, effects of GT3 on MSS- colon cancer cell lines will also be studied.
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Dave, Havya. "Effects Of Vitamin E Isomer, Gamma Tocotrienol (GT3), At Inhibiting Cell Growth And Inducing Apoptosis In Colon Cancer Cell Line HCT-116." Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/honors/128.

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Colorectal cancer is the third most prominent cancer world-wide and it is the second leading cause of cancer deaths in the United States. Many dietary components affect the risk of developing colorectal cancer, such as Vitamin E. Of the eight isomers of Vitamin E, four have a tocotrienol structure. Tocotrienols are found at highest concentrations in palm oil, which is ingested more in areas of Asia where the incidence of colorectal cancer is the lowest, suggesting a role of tocotrienols in the prevention of colorectal cancer. The metabolism of Arachidonic acid pathway produces a host of pro-inflammatory metabolites either by the Cyclooxygenase (Cox) pathway or the Lipoxygenase (Lox) pathway. The expression of Lox is increased in various human cancer lines; this over expression has been associated with tumor cell proliferation, resistance to apoptosis, and angiogenesis. Another important pathway related to cancer involves mTOR (mammalian target of rapamycin), which is involved in cell growth and human tumorigenesis. The focus of this study included treatment of the HCT-116 colon cancer cell line with gamma tocotrienol to examine potential pathways involved in the induction of apoptosis. Also, whether the Vitamin E-mediated signaling through Arachidonic acid metabolism is necessary for the down regulation of protein translation in the mTOR pathway by using chemical inhibitors specific to Arachidonic acid in the presence and absence of vitamin E treatment was explored. The colon cancer cell line, HCT-116, was treated with gamma tocotrienol isomer and then isolated at 18 and 24 hours. Cells lysates were analyzed by Western Blotting. Our data shows that the mTOR pathway is downregulated by treatment with gamma tocotrienol at 18 hours and 14 hours for 5 µM demonstrating that protein translation is abrogated. Phospho S6 ribosomal protein and phospho-p70 S6 kinase are both downregulated, and phospho-4EBP1 is up regulated upon treatment of gamma tocotrienol. Furthermore, at the same concentrations, Caspase 12 and Caspase 8 are cleaved indicating apoptosis. In addition, parallel up-regulation of 15-LOX-1 and down regulation of Cox-2 at 5 µM at 18 hours is observed. Upon treatment with Caffeic acid, 15-lox-1 is over expressed causing mTOR trend to reverse and down regulation of ERK. Thus, mTOR regulation is dependent on a delicate balance of fatty acid metabolites.
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Ju, Sy-Yeuan, and 朱思遠. "Elucidation of the role of CD44 in colon cancer stem cells derived from HCT-15 and HCT-116 lines and identification of drugs targeting this population." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/98156533506941235113.

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博士
國立陽明大學
生物藥學研究所
102
Cancer stem cells (CSCs) are known to play critical roles in tumor initiation and progression. Accumulating evidence also shows that CSCs are responsible for tumor relapse after chemotherapy. The purpose of this study was to isolate CSCs from established human colorectal carcinoma (CRC) cell lines, characterize them thoroughly and dissect the mechanism of their stemness. Additionally, identifying novel agents capable of specifically targeting colorectal cancer stem cells (CRSCs) that may improve CRC treatment is the other goal of this work. To reach the first aim, freshly isolated CD44+ and CD44- cells from the HCT-15 human CRC line were subjected to various analyses. Interestingly, CD44+ cells exhibited higher soft agar colony-forming ability and in vivo tumorigenicity than the CD44- ones. In addition, a significant upregulation of the protein level of Snail and a marked downregulation of miR-203, a stemness inhibitor, were found in CD44+ HCT-15 cells which suggested that this EMT activator and microRNA might be crucial for the generation and/or maintenance of CRSCs. Moreover, the levels of several other EMT inducers and miR-203 were found to be positively and negatively correlated with those of CD44, respectively, in both HCT-15 and HCT-116 cells. Interestingly, further analyses revealed that miR-203 levels were repressed by Snail, which was shown to bind directly to specific E-box(es) present in the miR-203 promoter. In agreement, silencing miR-203 expression in wild-type HCT-116 cells also resulted in an increase of their stemness. Finally, I discovered that c-Src kinase activity was required for the downregulation of miR-203 in HCT-15 cells, which was stimulated by the interaction between hyaluronan (HA) and CD44. With respect to the identification of agent(s) capable of selectively targeting CRSCs, I found that Compound X, was the most effective one among the compounds provided kindly by Professor Chi-Yin Huang of our Institute after a quick primary screening. In fact, Compound X could dose-dependently diminish the CRSC populations present in both HCT-15 and HT-29 cells as well as induce apoptosis of the CRSCs-enriched oxaliplatin-resistant HT-29 cells. Additionally, this Compound not only inhibited spheroid- and colony-forming abilities of HCT-15 and HT-29 cells drastically but also suppressed the expression of several well-defined pluripotency factors such as Oct4, Nanog, and Bmi1 as well as EMT inducers Snail and Twist. Moreover, Compound X could act synergistically with oxaliplatin to kill HCT-15 and HT-29 cells, especially their CD44+ populations. Finally, I showed that not only was the percentage of SC population decreased significantly but also the sensitivity to Compound X was notably reduced in both HT-29 and HCT-116 lines by RNAi-mediated silencing of transcriptional factor Y, an oncogenic transcription factor, a SC self-renewal promoter, and a well-defined target of this antibiotic. Taken together, this study shows that CD44 is critical for modulating stemness in CSCs, at least those present in HCT-15 and HCT-116 human CRC lines. More importantly, my results demonstrate that the downregulation of miR-203 mediated by HA/CD44 signaling is the main reason for stemness maintenance in the aforementioned CRSCs. In the meantime, I identify and validate the selective inhibitory effects of Compound X on various CRSCs although this antibiotic has already been shown to be active against a wide variety of types of tumors. Judging by its good synergism with oxaliplatin, Compound X may be used in combination with the clinically available chemotherapeutic drugs to improve CRC treatments.
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Szu-Wei, Huang, and 黃思瑋. "Dissecting the mechanisms underlying stemness reduction mediated by miR-203 in HT-29 and HCT-116 human colon cancer cells." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/77287063361485031527.

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碩士
國立陽明大學
生物藥學研究所
102
Cancer stem cells (CSCs) or tumor-initiating cells (TICs) are defined as a small subpopulation present in tumors responsible for the initiation, metastasis, recurrence and treatment resistance of a wide variety of cancers including colorectal carcinoma (CRC). Our previous study has shown that downregulated expression of miR-203 is crucial for the increased stemness of HCT-15 and HCT-116 human CRC cells triggered by the interaction between cell surface CD44 and its main ligand, hyaluronan (HA). However, the precise role(s) of miR-203 in modulating the stemness of these cells is largely undefined. To assess the contributions of miR-203 in colorectal cancer stem cells (CRSCs), miR-203-overexpressing and -sequestered stable clones derived from both HT-29 and HCT-116 human CRC cells were established, respectively. Supporting our previous observations, overexpression and sequestration of miR-203 resulted in a significant reduction and a marked increase of self-renewal in these cells, respectively. Moreover, overexpression of miR-203 in these cells also drastically reduced their anchorage- independent growth abilities. In addition, surface levels of CD44, a prominent CRSC marker, as well as mRNA and protein levels of several SC markers (i.e., Nanog, Oct-4 and Bmi1) in these cells were also inversely correlated with miR-203 levels. To further delineate the mechanism underlying the stemness-diminishing effects of miR-203, its potential targets were searched by miRWalk. Among those identified, GATA6 and IL-8 were the most interesting ones since their well-known roles in normal intestinal SCs and CRSCs, respectively. Subsequently, reporter assay using a luciferase gene fused with the 3' untranslated region (3'-UTR) of GATA6 mRNA confirmed that GATA6 was indeed a direct target of miR-203. In accordance, GATA6 knockdown in HT-29 and HCT-116 cells inhibited the expression of not only CD44 but also Lgr5, a newly identified GATA6 target which plays a crucial role in potentiating Wnt signaling in various SCs. Moreover, I found that increased Lgr5 expression in miR-203-sequestered clones was due mainly to GATA6 stimulation. In addition, the levels of Dickkopf-related protein 1 (DKK1), a Wnt antagonist known to be repressed by GATA6, were found to be significantly increased in miR-203-overexpressing HT-29 and HCT-116 cells, which might account at least in part for their stemness reduction. Fittingly, protein levels of β-catenin, the main mediator of Wnt signaling were also downregulated in miR-203-overexpressing and GATA6-knockdowned CRC cells. In the meantime, sphere-forming abilities marked decreases of IL-8 levels were detected in miR-203-overexpressing HT-29 cells whose could be partially restored by exogenous IL-8. Taken together, my data demonstrate that miR-203 suppresses the stemness of CRSCs present in HT-29 and HCT-116 lines by downregulating GATA6, resulting in diminished Wnt signaling due likely to a concomitant Lgr5 repression and DKK1 activation. In the meantime, reduced IL-8 production is also partially responsible for the stemness-inhibitory effects of this miR. .
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Shih, Ting-Ying, and 史亭瑩. "Sulforaphane induces cell death through the G2/M phase arrest and apoptosis by reactive oxygen species dependent pathway in human colon cancer HCT 116 cells." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/ny966u.

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碩士
中國醫藥大學
醫學檢驗生物技術學系碩士班
102
Sulforaphane (SFN) is a rather simple organic compound that is found in the largest concentrations in the cruciferous or mustard family of plants, including broccoli, cauliflower, and cabbage. It has been reported to exhibit a wide variety of biological activities including antioxidant, prevent and treat arthritis, protect against respiratory ailments and prevention of heart disease effects. In addition, it has been shown to inhibit the proliferation and to induce the apoptosis of a wide variety of tumor cells including breast, prostate and lung cancers. However, it is still unclear whether SFN effectively induces apoptotic cell death of human colon cancer HCT 116 cells. Herein, HCT 116 cells were treated with different concentrations of SFN for a specific time period and investigated for effects on apoptosis analyses. Our results indicated that HCT 116 cells after exposure to SFN significantly decreased cell viability, induced cell morphological changes, DNA damage, fragment and cause G2/M phase arrest. Western blotting results indicated that SFN inhibit cyclin A and cdk1 expressions and promoted chk-1 and chk-2 levels that were caused G2/M phase arrest. Flow cytometry assay indicated that SFN promoted calcium productions, increased percentage of early apoptotic cells and loss of mitochondrial membrane potential and resulted from cell death pathway such as the Caspase-3, -8, -9 active form and changed protein levels of Bcl-2 family in HCT 116 cells. Western blot analytics proved the increase of pro-apoptotic proteins such as Bax, AIF, Endo G, Cytochrome c, Caspase-3, and the declined the anti-apoptotic proteins, such as Bcl-2, XIAP, Mcl-1. In the future, SFN may be useful for developing new therapeutic regimens for the treatment of human colon cancer.
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Li, Tain-Yu, and 李天佑. "Tea extract (EGCG or TF-3-G) inhibits cell cycle progression through JNK signaling in HCT-116 human colorectal cancer cell line." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/85705898222279799620.

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碩士
中山醫學大學
口腔科學研究所
101
Catechins in cancer-related research have received great attention in recent years. The (-)-epigallocatechin-3-gallate (EGCG) are most abundant compound in extracted that effective inhibits the growth of cancer cells. Theaflavins extracted from completely fermented black tea are also inhibits the growth of cancer cells effectively. In this study, we use human colorectal cancer cell lines that were treated with tea extracts such as EGCG or TF-3-G, and their effects on the HCT116 cells were investigated. EGCG or TF-3-G inhibits the growth of HCT-116 cells through triggering the G2/M arrest in HCT-116. We further examined cellular-signaling protein and found that EGCG or TF3-G increase the activities of JNK and also p53 and p21 expression, but reduces Cyclin A and Cyclin B expression. HCT-116 cells pre-treated with JNK Inhibitor (SP600125) before adding EGCG or TF-3-G were examined and we found that EGCG or TF-3-G is able to reverse G2/M arrest in HCT-116, wherein p53, p21, cyclin A and cyclinB protein levels are not significantly changed comparison to cells without treated EGCG or TF-3-G. We found that EGCG or TF-3-G inhibits HCT-116 cells growth through mechanisms that influence on the activity of JNK signaling pathway, and future change cyclin A and Cyclin B expression levels to induce cell cycle arrest.
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Book chapters on the topic "HCT-116 cells"

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Skonieczna, Magdalena, Dorota Hudy, Patryk Bil, Malgorzata Adamiec, Marta Stachowska, and Krzysztof Biernacki. "Role of Let-7 Family miRNAs in Migration of Colorectal Cancer HCT 116 and Caco-2 Cells After Stimulation by the Adipokine Vaspin. Time-Lapse Live-Cell Microscopic Observations." In Advances in Intelligent Systems and Computing, 47–61. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-29885-2_5.

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Patil, Poounima, and Suresh Killedar. "Colon Available Bioactive Compounds Exhibits Anticancer Effect on In-Vitro Model of Colorectal Cancer." In Biosynthesis [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96632.

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The current work was addressed to characterize gallic acid from amla fruit and quercetin from peels of pomegranate fruit and formulated into Chitosan (CS) nanoparticles and to evaluate their cytotoxicity towards human colorectal cancer (HCT 116) cell lines. Identification of the biomolecules was performed by chromatographic and spectroscopic techniques and characterization of gallic acid and quercetin loaded chitosan nanoparticles carried out by using FT-IR, X- ray diffraction, entrapment efficiency and loading content confirmed successful encapsulation of biomolecules into nanoparticles. In vitro drug release studies done by using simulated fluids at various pH (1.2, 4.5, 7.5, and 7.0) to mimic the GIT tract and achieved drug releases 77.56% for gallic acid 79.06% for quercetin at 24 hr. in a sustained manner. The human HCT116 cell line by MTT assay results inferred that the synthesized CS nanoparticles demonstrated shows more effective antiproliferative potential with IC50 value of 36.17 ug/ml than polyherbal extract 60.32ug/ml.
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Conference papers on the topic "HCT-116 cells"

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Šeklić, Dragana, Milena Jovanović, Nevena Milivojević, and Marko Živanović. "PLATINUM(IV) COMPLEX AND ITS CORRESPONDING LIGAND SUPPRESS CELL MOTILITY AND PROMOTE EXPRESSION OF FRIZZLED-7 RECEPTOR IN COLORECTAL CANCER CELLS." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.288s.

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Suppression of cell movement is an imperative in the effectiveness of future generations of chemotherapeutics. Frizzled 7 receptor (FZD7), as the first protein of Wnt/β-catenin signaling cascade, plays a significant role in regulation of cell differentiation, proliferation, and cell migration. This study aimed to investigate the potential effects of platinum (IV) complex: [PtCl4 (dbu-S, S-eddp)] – C1, and its corresponding ligand – L1 on cell movement, as well as the FZD7 expression and localization after treatments on two human colorectal carcinoma cell lines (HCT-116, SW-480). A Wound healing assay was used to examine cell migration, while FZD7 protein expression was examined by immunofluorescence. Chemical compounds, especially L1, reduced cell motility of both tested cell lines. They showed a particularly good effect on HCT-116 cells, increasing protein expression of the antimigratory marker FZD7 whose localization was observed on the cell membrane of HCT-116 cells. Suppression of cell movement was significantly lower in SW-480 cells after treatments, when compared to HCT-116, with an obvious decrease of FZD7 receptor expression and its localization in the cytoplasm of these cells. Our results indicate that among the examined treatments, the ligand showed more significant results in the suppression of HCT-116 cell movement, most likely through the stimulation of differentiation, which is indicated by the promotion of FZD7 expression.
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Jovanović, Milena M., Katarina Virijević, Jelena Pavić, Dejan Arsenijević, Katarina Pecić, Nikolina Kastratović, Marko Živanović, and Dragana Šeklić. "Antimigratory Activity of Royal Jelly on HCT-116 Colorectal Cancer Cells." In Foods 2022. Basel Switzerland: MDPI, 2022. http://dx.doi.org/10.3390/foods2022-12951.

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Dachineni, Rakesh, Goqiang Ai, and Jayarama B. Gunaje. "Abstract 3501: Aspirin modulates oncogene expression in hct 116 colon cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3501.

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Subroto, Priscilla Aya Maheswari, Ade Arsianti, Trivani Putri, and Elvira Lesmana. "Phytochemical analysis and anticancer activity of seaweed Eucheuma Sp. against colon HCT-116 cells." In SECOND INTERNATIONAL CONFERENCE OF MATHEMATICS (SICME2019). Author(s), 2019. http://dx.doi.org/10.1063/1.5096719.

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Gursoy, Duygu. "Anti-cancer effect of Mirtazapine against MCF-7, HCT-116 and MiaPaCa-2 cancer cells." In 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-121.

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Gunaje, Jayarama B., Srinivasan Marimuthu, Raghavender S. V. Chivukula, Majid Moridani, Fred K. Hagen, and Lloyd F. Alfonso. "Abstract 1638: Aspirin acetylates multiple cellular proteins in HCT-116 cells: Identification of novel targets." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1638.

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Alfonso, Lloyd F., Raghavender Chivukula, Srinivasan Marimuthu, and Jayarama B. Gunaje. "Abstract 5041: Aspirin acetylates and activates p53 in HT-29 and HCT-116 colon cancer cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5041.

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Milenković, Dejan A., Marko N. Živanović, Milan S. Dekić, Marijana Stanojević Pirković, and Jelena R. Đorović Jovanović. "CYTOTOXIC ACTIVITY AND MOLECULAR DOCKING STUDY OF 4- SUBSTITUTED FLAVYLIUM SALT." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.466m.

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In the present manuscript, the cytotoxic activity of flavylium cation substituted at 4- position with phenyl (FC-4Ph) was tested to two cells lines (human colorectal carcinoma, HCT-116, and human fibroblast lung, MRC-5). In vitro cytotoxicity experiments were performed to elucidate the possible anticancer activity of tested substance. Investigated compound did not show cytotoxic effect on HCT-116 after 24 h, while after 72 h exerted significant effect. A significant selectivity towards colorectal carcinoma cells was observed. On the other hand, this compound did not show any effect on MRC-5 cell line. The molecular interactions between receptor tyrosine kinase (RTK) and title compound was examined. The crystal structure of investigated receptor RTK was downloaded from Protein Data Bank. The native bound ligand ((E)-[4-(3,5-difluorophenyl)-3H-pyrrolo[2,3-b]pyridin-3-ylidene](3- methoxyphenyl)methanol was extracted from receptor and binding pocket analysis was performed. Re-docking was carried out with the FC-4Ph in order to generate the same docking pose as found in co-crystallized form of receptor. The obtained results of revealed that investigated compound binds at the same binding pockets to RTK, as well as native bound ligand, by weak non-covalent interactions. The most prominent interactions are hydrogen bonds, π-alkyl, and π-π interactions. The preliminary results suggest that investigated compound showed good binding affinity against RTK, as evident from the free binding energy (ΔGbind in kJ/mol).
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Alotaibi, Moureq R., Matthew J. Beckman, Xu Di, Ray Lee, and David A. Gewirtz. "Abstract 3957: Cell death and growth arrest pathways mediating the actions of stilbene 5C in HCT-116 colon cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3957.

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Alotaibi, Moureq R. "Abstract 1658: Cell death and growth arrest pathways mediating the actions of stilbene 5c in HCT-116 colon cancer cells and B16F10 melanoma cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1658.

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