Oct 2026· Molecular Carcinogenesis· 0 citations· 30 references
Medicine
TL;DR
It is demonstrated that USP26 functions as an oncogenic driver in NSCLC by stabilizing Gαs and suppressing autophagy, highlighting its potential as a prognostic biomarker and therapeutic target.
Abstract
Non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related mortality worldwide. Ubiquitin-specific protease 26 (USP26) has been implicated in tumor progression, but its functional role and molecular mechanism in NSCLC remain poorly understood. USP26 was significantly upregulated in NSCLC tissues and cell lines, correlating with poor prognosis. Functionally, USP26 promoted cell proliferation and colony formation while inhibiting apoptosis. Mechanistically, USP26 directly interacted with and deubiquitinated Gαs, stabilizing it to activate the cAMP/PKA signaling pathway. USP26 also suppressed autophagic flux and ER-phagy, and its pro-tumor effects were abrogated by the autophagy inhibitor 3-MA. Our findings demonstrate that USP26 functions as an oncogenic driver in NSCLC by stabilizing Gαs and suppressing autophagy, highlighting its potential as a prognostic biomarker and therapeutic target.
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