Matrine triggers colon cancer cell apoptosis and G0/G1 cell cycle arrest via mediation of microRNA‐22

2020 ◽  
Vol 34 (7) ◽  
pp. 1619-1628 ◽  
Author(s):  
Jiao Liu ◽  
Yazhuo Guo ◽  
Jing Cao
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Colon Cancer Cell ◽  
Cancer Cell Apoptosis ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

scholarly journals Superior Inhibitory Efficacy of Butyrate over Propionate and Acetate Against Human Colon Cancer Cell Proliferation via Cell Cycle Arrest and Apoptosis

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 364-364
Author(s):  
Huawei Zeng ◽  
Stephanie Hamlin ◽  
Bryan Safratowich ◽  
Wen-Hsing Cheng ◽  
LuAnn Johnson
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Hct116 Cell ◽  
Colon Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Human Colon Cancer ◽  
Cycle Arrest

Abstract Objectives Intake of fiber has beneficial properties for gut health. These effects may be due to the increased production of short chain fatty acids (SCFAs) such as acetate, propionate and butyrate during dietary fiber fermentation in the colon. We tested the hypothesis that butyrate exhibits a stronger inhibitory potential against colon cancer cell proliferation compared with acetate and propionate. Methods With a human HCT116 colon cancer cell culture model, we used cell cycle, apoptosis, PCR array, biochemical, western blotting and immunofluorescent assays to determine SCFAs’ inhibitory effects on HCT116 cell proliferation. Results We determined the half maximal inhibitory concentrations (IC50) of SCFAs in HCT116 cell proliferation by examining cell growth curves. At 24- and 48- hour time points, IC50 (mM) concentrations of acetate, propionate and butyrate were [66.0 and 29.0], [9.2 and 3.6] and [2.5 and 1.3], respectively.  Consistent with the greater anti-proliferative effect, butyrate exhibits >3-fold stronger potential for inducing cell cycle arrest (including c-Myc/p21 signaling) and apoptosis when compared with acetate and propionate. Subsequently, we focused on the effect of butyrate on apoptotic gene expression. Using a PCR array analysis, we identified 17 pro-apoptotic genes, 6 anti-apoptotic genes, and 4 cellular mediator genes with >1-fold increase or decrease in mRNA levels out of 93 apoptosis related genes in butyrate-treated HCT116 cells when compared with untreated HCT116 cells. These genes were mainly involved in the tumor necrosis factor alpha receptor, NFκB, caspase recruitment domain-containing protein and B-cell lymphoma-2 regulated pathways. Conclusions Collectively, we demonstrated a greater inhibitory efficacy of butyrate over propionate and acetate against human colon cancer cell proliferation via cell cycle arrest and apoptosis. Funding Sources This work was supported by U.S. Department of Agriculture, Agricultural Research Service, research project 3062–51,000-056–00D.

Lentivirus-mediated siRNA targeting SAE1 induces cell cycle arrest and apoptosis in colon cancer cell RKO

2014 ◽  
Vol 48 (1) ◽  
pp. 91-98 ◽  
Author(s):  
N. Song ◽  
X. -D. Gu ◽  
Y. Wang ◽  
Z. -Y. Chen ◽  
L. -B. Shi
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Cycle Arrest

scholarly journals Treatment of Breast and Colon Cancer Cell Lines with Anti-Helmintic Benzimidazoles Mebendazole or Albendazole Results in Selective Apoptotic Cell Death

2021 ◽  
Author(s):  
Jakeb SSM Petersen ◽  
Sarah Baird
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Cycle Arrest ◽  
Colon Cancer Cell Lines ◽  
Ht 29

Abstract Purpose: Anti-helmintic drugs mebendazole and albendazole are commonly used to treat a variety of parasitic infestations. They have recently shown some promising results in pre-clinical in vitro and in vivo anti-cancer studies. We compare their efficacy in breast and colon cancer cell lines as well as in non-cancerous cells and elucidate their mechanism of action. Methods: The drugs were screened for cytotoxicity in MDA-MB-231, MCF-7 (breast cancer), HT-29 (colorectal cancer) and mesenchymal stem cells, using the MTT assay. Their effects on the cell cycle, tubulin levels and cell death mechanisms were analysed using flow cytometry and fluorescent microscopy. Results: Mebendazole and albendazole were found to selectively kill cancer cells, being most potent in the colorectal cancer cell line HT-29, with both drugs having IC50 values of less than 1 µM at 48 hours. Both mebendazole and albendazole induced classical apoptosis characterised by caspase-3 activation, phosphatidylserine exposure, DNA fragmentation, mitochondrial membrane permeability and reactive oxygen species production. Cell cycle arrest in the G2/M phase was found, and tubulin polymerisation was disrupted.Conclusion: Mebendazole and albendazole cause selective cancer cell death via a mechanism of classical apoptosis and cell cycle arrest, which involves the destabilisation of microtubules.

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