Abstract
Exopolysaccharides (EPS) from lactic acid bacteria (LAB) have been reported to play vital parts in the modulation of cell-cycle and apoptosis in cancer cells. However, the mechanisms by which EPS regulate the proliferation and apoptosis of cancer cells remain incompletely understood. We thus used different cancer cells to evaluate the anticancer ability and to investigate the underlying molecular mechanism of EPS from Lactobacillus plantarum NCU116 (EPS116). Our studies showed that EPS116 inhibited the proliferation of cancer cells in a cell type manner, and remarkably repressed the growth and survival of CT26 through induction of apoptosis. Moreover, EPS116 increased the expression of pro-apoptotic genes, including Fas, Fasl and c-Jun, induced the phosphorylation of c-Jun in CT26 cells. Furthermore, TLR2 (Toll like receptor 2) was upregulated by EPS116, and the CT26 cells with TLR2 knockdown were found to be insensitive to EPS116, suggesting that the anti-cancer activity of EPS116 may be TLR2-dependent. Taken together, the suppressive efficacy of EPS116 on the proliferation of CT26 cells may be mediated via TLR2 and the activation of c-Jun dependent Fas/Fasl-mediated apoptotic pathway. Our study has, for the first time, shown that EPS from LAB induced c-Jun dependent Fas/Fasl-mediated apoptosis via TLR2 in CT26 cells.
Highlights
Cancer is a class of diseases that are featured of the uncontrolled proliferation of cells with invasive and motile ability
We found that EPS from Lactobacillus plantarum NCU116 (EPS116) induced the apoptosis of CT26 cells via TLR2 and c-Jun dependent Fas/ Fasl-mediated apoptotic pathway
The homogeneity and the average molecular weight (MW) of EPS116 were analyzed by high performance gel permeation chromatography (HPGPC)
Summary
Cancer is a class of diseases that are featured of the uncontrolled proliferation of cells with invasive and motile ability. These findings imply that the activation of TLR2 on the intestinal cancer cells by EPS may have a direct role in inducing apoptosis. We found that EPS116 induced the apoptosis of CT26 cells via TLR2 and c-Jun dependent Fas/ Fasl-mediated apoptotic pathway.
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