Fungal Immunomodulatory Protein from Nectria haematococca Suppresses Growth of Human Lung Adenocarcinoma by Inhibiting the PI3K/Akt Pathway

文献类型： 外文期刊

第一作者： Xie, Yingying

作者： Xie, Yingying;Li, Shuying;Liu, Shujun;Wang, Fengzhong;Wen, Boting;Sun, Lichao;Cao, Hao;Jia, Ning;Gu, Tianyi;Xin, Fengjiao;Sun, Lei;Fang, Xiangdong;Lou, Xiaomin;Sun, Lei;Fang, Xiangdong;Lou, Xiaomin;Sun, Lei;Fang, Xiangdong;Lou, Xiaomin;Chai, Yushuang

作者机构：

关键词： fungal immunomodulatory protein; Nectria haematococca; lung adenocarcinoma; PI3K; Akt; apoptosis; autophagy; cell cycle arrest

期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：5.923； 五年影响因子：6.132 ）

ISSN： 1422-0067

年卷期： 2018 年 19 卷 11 期

页码：

收录情况： SCI

摘要： Lung cancer is a common disease that is associated with poor prognosis. Fungal immunomodulatory protein from Nectria haematococca (FIP-nha) has potential as a lung cancer therapeutic; as such, illuminating its anti-tumor mechanism is expected to facilitate novel treatment options. Here, we showed that FIP-nha affects lung adenocarcinoma growth ex vivo and in vivo. Comparative quantitative proteomics showed that FIP-nha negatively regulates PI3K/Akt signaling and induces cell cycle arrest, autophagy, and apoptosis. We further demonstrated that FIP-nha suppresses Akt phosphorylation, leading to upregulation of p21 and p27 and downregulation of cyclin B1, cyclin D1, CDK2, and CDK4 expression, ultimately resulting in G1/S and G2/M cell cycle arrest. Meanwhile, FIP-nha-induced PI3K/Akt downregulation promotes A549 apoptosis by increasing the expression ratio of Bax/Bcl-2 and c-PARP and autophagy by decreasing the phosphorylation of mTOR. Thus, we comprehensively revealed the anti-tumor mechanism of FIP-nha, which inhibits tumor growth by modulating PI3K/Akt-regulated cell cycle arrest, autophagy, and apoptosis, and provided the basis for further application of fungal immunomodulatory proteins, especially FIP-nha.

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