Cordyceps sinensis polysaccharide inhibits colon cancer cells growth by inducing apoptosis and autophagy flux blockage via mTOR signaling

被引:86
作者
Qi, Wucheng [1 ]
Zhou, Xingtao [1 ]
Wang, Junqiao [1 ]
Zhang, Ke [1 ]
Zhou, Yujia [1 ]
Chen, Shuping [1 ]
Nie, Shaoping [1 ]
Xie, Mingyong [1 ,2 ]
机构
[1] Nanchang Univ, State Key Lab Food Sci & Technol, China Canada Joint Lab Food Sci & Technol Nanchan, 235 Nanjing East Rd, Nanchang 330047, Jiangxi, Peoples R China
[2] Jiangxi Normal Univ, Natl R&D Ctr Freshwater Fish Proc, Nanchang 330022, Jiangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
Cordyceps sinensis polysaccharide; Autophagy; Apoptosis; Colon cancer cell; mTOR signaling; PROTEIN; MODULATION; DEATH;
D O I
10.1016/j.carbpol.2020.116113
中图分类号
O69 [应用化学];
学科分类号
081704 ;
摘要
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.
引用
收藏
页数:11
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