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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.

植物乳杆菌 EPS116 通过 TLR2 调控 c-Jun/Fas/Fasl 信号通路诱导 CT26 细胞凋亡

乳酸菌来源的胞外多糖（EPS）被报道在调节癌细胞的细胞周期和凋亡中发挥重要作用。然而，EPS 调节癌细胞增殖和凋亡的机制尚不完全清楚。因此，我们使用不同的癌细胞来评估 EPS116 的抗癌能力，并研究其潜在的分子机制。我们的研究表明，EPS116 以细胞类型依赖的方式抑制癌细胞的增殖，并通过诱导细胞凋亡显著抑制 CT26 的生长和存活。此外，EPS116 增加了促凋亡基因 Fas、Fasl 和 c-Jun 的表达，诱导 CT26 细胞中 c-Jun 的磷酸化。此外，EPS116 上调了 TLR2（Toll 样受体 2）的表达，而 TLR2 敲低的 CT26 细胞对 EPS116 不敏感，表明 EPS116 的抗癌活性可能依赖于 TLR2。综上所述，EPS116 对 CT26 细胞增殖的抑制作用可能是通过 TLR2 及其激活 c-Jun 依赖性 Fas/Fasl 介导的凋亡途径介导的。本研究首次表明，LAB 产生的 EPS 通过 TLR2 在 CT26 细胞中诱导 c-Jun 依赖性 Fas/Fasl 介导的凋亡。