Effects And Improvement Mechanism Of Short-Chain Fatty Acids On Colon Cancer

Colon cancer is a malignant tumor,which makes the life of colon cancer patients a huge threat.Some studies have shown that the addition of dietary fiber to the daily diet can prevent colon cancer to some extent.In this experiment,two colon cell lines,colon cancer cell line HCT116 and human normal colonic epithelial cell FHC were used.Normal colonic cell cycle arrest and promotion of apoptosis.From the cell cycle and apoptosis-related genes and proteins as the detection target,sodium acetate,sodium propionate,sodium butyrate in a certain concentration range and intervention time to improve the role of colon cancer.The experimental results can be summarized as follows:After 48 hours of sodium acetate intervention,it was observed under the microscope that there were more floating cells in the culture medium of colon cancer cells starting at 30 mM.In the experiment,the number of low-concentration sodium acetate cells below 1 mM increased.Cell cycle experiments showed that 1 mM sodium acetate had a certain promoting effect on colon cancer cell proliferation and had no obvious blocking effect on cell cycle.It is speculated that sodium acetate will accelerate,The vigorous anabolism of tumor cells accelerates their proliferation.The slope of the proliferation curve of 5 mM sodium propionate intervention cells became smaller,indicating that the cells grew slowly,and the cells basically stopped growing under the intervention of 15 mM sodium propionate.The same inhibition of proliferation effect.When the concentration of sodium propionate was more than 5 mM,the cyclin b1 in HCT116 cells was down-regulated compared with the uninterrupted cells,which caused G2/M phase arrest in colon cancer cells.The cyclin b1 in FHC cells was up-regulated,indicating that the concentration was higher.Propionate acts as a source of energy for normal colonic epithelial cells and promotes mitosis.Therefore,in this experiment,the optimal concentration of sodium propionate to improve colon cancer is 5 mM.Inhibition of butyrate at a concentration greater than 1 mM for 24 h and above induced apoptosis and inhibited proliferation of HCT116 cells.HCT116 cells showed a greater apoptotic response than FHC cells that were not sensitive to butyric acid,and strong antiproliferative effects were observed in FHC cells.After 48 h,2 mM butyrate-induced HCT116 cells had very significant G2/M phase arrest in butyrate-treated HCT116 cells compared to normal colonic epithelial FHC.Butyrate induces colon cancer cell growth arrest by regulating the expression of cell cycle regulators p21 and gadd45,and arrests cancer cells by increasing the cyclin-dependent kinase inhibitor p21 and decreasing the cyclin gene cyclin b1.G2/M period.The results of the above studies showed that these three short-chain fatty acids induced apoptosis in colon cancer cells in a time-dependent manner,in which sodium butyrate had a dose-dependent apoptosis of colon cancer cells,and sodium propionate had the best at 5 mM.The effect of the intervention and sodium acetate did not promote apoptosis in colon cancer cells in a low concentration range.