NOS1 S-nitrosylates PTEN and inhibits autophagy in nasopharyngeal carcinoma cells

• DOI: 10.1038/cddiscovery.2017.11
• Publication Date: 2017-02-20T10:54:30Z
• Authors: Lingqun Zhu; Linlin Li; Qianbing Zhang; Xiao Yang; Zhiwei Zou; Bingtao Hao; Francesco M Marin...; Zhengjun Liu; Zhuo Zhong; Meng Wang; Xiaoxuan Li; Qianli Wang; Keyi Li; Wenwen Gao; Kaitai Yao; Qiuzhen Liu
• Keywords: 0303 health sciences; 03 medical and health sciences; Article; 3. Good health

Abstract Autophagy is a cellular survival mechanism that involves the catabolic degradation of damaged proteins and organelles during periods metabolic stress, when overly stimulated, commonly contributes to cell death. Nitric oxide (NO), potent messenger, participates in complex which assists controlling autophagy. However, by endogenous NO formed distinct isoforms nitric synthase (NOS) helps regulate autophagy cancer cells remains unclear. Here we report NOS1 reduces excessive levels promotes nasopharyngeal carcinoma cells. We found inhibition increased death resulting from siRNA or use pharmacologic agents; this effect was reversed inhibitor, chloroquine. The role process depended on activation AKT/mTOR signaling S -nitrosylation phosphatase tensin homolog (PTEN) proteins. modifies PTEN protein might involve direct interaction between these two molecules. Moreover, an vivo study, inhibitor N(G)-nitro- L -arginine methyl ester activated promoted xenograph tumors. Our studies demonstrated prevents via PTEN, pathway. pathway are promising targets for improving chemotherapeutic treatment cancer.