scholarly journals CBX3 promotes colon cancer cell proliferation by CDK6 kinase-independent function during cell cycle

Oncotarget ◽  
2017 ◽  
Vol 8 (12) ◽  
pp. 19934-19946 ◽  
Author(s):  
Yao Fan ◽  
Haiping Li ◽  
Xiaolong Liang ◽  
Zheng Xiang
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Independent Function

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.

scholarly journals Palmitoylethanolamide Reduces Colon Cancer Cell Proliferation and Migration, Influences Tumor Cell Cycle and Exerts In Vivo Chemopreventive Effects

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1923
Author(s):  
Ester Pagano ◽  
Tommaso Venneri ◽  
Giuseppe Lucariello ◽  
Donatella Cicia ◽  
Vincenzo Brancaleone ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Cancer Cell ◽  
Colon Carcinogenesis ◽  
Cyclin B1 ◽  
Colon Cancer Cell ◽  
Cancer Cell Proliferation

Palmitoylethanolamide (PEA) is an endogenous fatty acid amide related to the endocannabinoid anandamide. PEA exerts intestinal anti-inflammatory effects, but knowledge of its role in colon carcinogenesis is still largely fragmentary. We deepened this aspect by studying the effects of PEA (ultramicronized PEA, um-PEA) on colon cancer cell proliferation, migration and cell cycle as well as its effects in a murine model of colon cancer. Results showed that um-PEA inhibited tumor cell proliferation via peroxisome proliferator-activated receptor α and G protein-coupled receptor 55, induced cell cycle arrest in the G2/M phase, possibly through cyclin B1/CDK1 upregulation, and induced DNA fragmentation. Furthermore, um-PEA reduced tumor cell migration by reducing MMP2 and TIMP1 expression. In vivo administration of um-PEA exerted beneficial effects in the azoxymethane model of colonic tumors, by reducing the number of preneoplastic lesions and tumors. Collectively, our findings provide novel proofs on the effects of um-PEA in colon carcinogenesis.

NF-κB regulates colon cancer cell proliferation and tumorigenicity

2001 ◽  
Vol 120 (5) ◽  
pp. A615-A615
Author(s):  
S KUWADA ◽  
C SCAIFE ◽  
J KUANG ◽  
R DAYNES
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Cancer Cell Proliferation

Cellular mechanisms involved in the melatonin inhibition of HT-29 human colon cancer cell proliferation in culture

2007 ◽  
Vol 43 (2) ◽  
pp. 195-205 ◽  
Author(s):  
Ana García-Navarro ◽  
Cristina González-Puga ◽  
Germaine Escames ◽  
Luis C. López ◽  
Ana López ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Human Colon Cancer Cell ◽  
Cellular Mechanisms ◽  
Human Colon Cancer ◽  
Ht 29
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