PTEN S-nitrosylation by NOS1 inhibits autophagy in NPC cells

摘要

Nitric oxide synthases are ubiquitous enzymes inmalignant tumors, and known to exert both pro-tumorand anti-tumor effects. Endogenous NO is formed bythree NOS isoforms (NOS1, NOS2 and NOS3) thatdiffer in the way they modify transcription processesand enzyme activity1. it is a ubiquitous messengermolecule capable of regulating multiple cellularsignaling pathways2,including those which modulateautophagy3. Protein S-nitrosylation is a covalent posttranslational modification that results from coupling anitric oxide (NO) moiety containing a reactivethiol group to a protein cysteine residue to form anS-nitrosothiol (SNO) moiety4. S-nitrosylation plays akey role in the transmission of NO-based cellularsignals involved in vital cellular processes, includingtranscription regulation, DNA repair, apoptosis, andautophagy5.