State Key Laboratory of Food Science and Technology, China-Canada Joint Lab of Food Science and Technology (Nanchang), Nanchang University, 235 Nanjing East Road, Nanchang, Jiangxi, 330047, China.
State Key Laboratory of Food Science and Technology, China-Canada Joint Lab of Food Science and Technology (Nanchang), Nanchang University, 235 Nanjing East Road, Nanchang, Jiangxi, 330047, China.
Carbohydr Polym. 2020 Jun 1;237:116113. doi: 10.1016/j.carbpol.2020.116113. Epub 2020 Mar 4.
Cordyceps sinensis is thought to have anti-cancer effects, but its mechanisms remain elusive. In this study, we aimed to investigate the anti-cancer effect of Cordyceps sinensis polysaccharide (CSP) on human colon cancer cell line (HCT116) and its mechanism. Results indicated that CSP significantly inhibited the proliferation of HCT116 cells, increased autophagy and apoptosis, while blocked autophagy flux and lysosome formation. Further experiments showed that CSP decreased the expression of PI3K and phosphorylation level of AKT and mTOR, increased the expression of AMPKa and phosphorylation level of ULK1. In addition, repression of CSP-induced autophagy by bafilomycin (autophagy inhibitor) enhanced apoptosis and cell death of HCT116 cells. Hence, our findings suggested that CSP inhibited the proliferation of HCT116 cells by inducing apoptosis and autophagy flux blockage, which might be achieved through PI3K-AKT-mTOR and AMPK-mTOR-ULK1 signaling. CSP may be a potential therapeutic agent for colon cancer.
蛹虫草被认为具有抗癌作用,但作用机制尚不清楚。本研究旨在探讨蛹虫草多糖(CSP)对人结肠癌细胞(HCT116)的抗癌作用及其机制。结果表明,CSP 显著抑制 HCT116 细胞的增殖,增加自噬和细胞凋亡,同时阻断自噬流和溶酶体形成。进一步的实验表明,CSP 降低了 PI3K 的表达和 AKT 和 mTOR 的磷酸化水平,增加了 AMPKa 的表达和 ULK1 的磷酸化水平。此外,通过巴弗洛霉素(自噬抑制剂)抑制 CSP 诱导的自噬增强了 HCT116 细胞的凋亡和细胞死亡。因此,我们的研究结果表明,CSP 通过诱导细胞凋亡和自噬流阻断来抑制 HCT116 细胞的增殖,这可能是通过 PI3K-AKT-mTOR 和 AMPK-mTOR-ULK1 信号通路实现的。CSP 可能是一种治疗结肠癌的潜在药物。