2. Academic Validation
  3. Cordyceps sinensis polysaccharide inhibits colon cancer cells growth by inducing apoptosis and autophagy flux blockage via mTOR signaling

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

  • Carbohydr Polym. 2020 Jun 1;237:116113. doi: 10.1016/j.carbpol.2020.116113.
Wucheng Qi 1,  Xingtao Zhou 2,  Junqiao Wang 1,  Ke Zhang 1,  Yujia Zhou 1,  Shuping Chen 1,  Shaoping Nie 1,  Mingyong Xie 3
Affiliations

Affiliations

  • 1 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.
  • 2 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. Electronic address: [email protected].
  • 3 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; National R&D Center for Freshwater Fish Processing, Jiangxi Normal University, Nanchang, Jiangxi, 330022, China. Electronic address: [email protected].
PMID: 32241434 DOI: 10.1016/j.carbpol.2020.116113
Abstract

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.

Keywords

3-Methyladenine (PubChem CID: 135398661); Apoptosis; Autophagy; Bafilomycin A1 (PubChem CID: 6436223); Colon cancer cell; Cordyceps sinensis polysaccharide; Rapamycin (PubChem CID: 5284616); mTOR signaling.

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