biostudies-literatureGao WNatural Science Foundation of Guangdong ProvinceNational Natural Science Foundation of China408https://www.ebi.ac.uk/biostudies/studies/S-EPMC8050300biostudies-literatureUnknown12(4)One of the malignant transformation hallmarks is metabolism reprogramming, which plays a critical role in the biosynthetic needs of unchecked proliferation, abrogating cell death programs, and immunologic escape. However, the mechanism of the metabolic switch is not fully understood. Here, we found that the S-nitrosoproteomic profile of endogenous nitrogen oxide in ovarian cancer cells targeted multiple components in metabolism processes. Phosphofructokinase (PFKM), one of the most important regulatory enzymes of glycolysis, was S-nitrosylated by nitric oxide synthase NOS1 at Cys351. S-nitrosylation at Cys351 stabilized the tetramer of PFKM, leading to resist negative feedback of downstream metabolic intermediates. The PFKM-C351S mutation decreased the proliferation rate of cultured cancerCell death & diseaseThe role of S-nitrosylation of PFKM in regulation of glycolysis in ovarian cancer cells.PMC80503002017GC0106482018A0303137903197083681472834Zhang HHuang MLiu QLin YWei ZShen HZhang QJia JWang MZou ZWang QNie ZChen XZeng SXu PChen JJi KYang BLi KLi LRong ZZhu PZhu LYe SGao WHao BXu YfalseThe role of S-nitrosylation of PFKM in regulation of glycolysis in ovarian cancer cells.One of the malignant transformation hallmarks is metabolism reprogramming, which plays a critical role in the biosynthetic needs of unchecked proliferation, abrogating cell death programs, and immunologic escape. However, the mechanism of the metabolic switch is not fully understood. Here, we found that the S-nitrosoproteomic profile of endogenous nitrogen oxide in ovarian cancer cells targeted multiple components in metabolism processes. Phosphofructokinase (PFKM), one of the most important regulatory enzymes of glycolysis, was S-nitrosylated by nitric oxide synthase NOS1 at Cys351. S-nitrosylation at Cys351 stabilized the tetramer of PFKM, leading to resist negative feedback of downstream metabolic intermediates. The PFKM-C351S mutation decreased the proliferation rate of cultured cancer2021-01-01T00:00:00Z2021 Apr2026-05-08T21:28:27.651Z2022-02-09T17:58:46.537ZS-EPMC80503003385918610.1038/s41419-021-03681-0