USP1 promotes pancreatic cancer progression and autophagy by deubiquitinating ATG14.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is characterized by extremely poor prognosis, high mortality, and limited therapeutic strategy. Autophagy is hyperactivated in PDAC, and targeting autophagy is emerging as a promising therapeutic strategy. The dysfunction of deubiquitinase ubiquitin-specific peptidase 1 (USP1) results in tumorigenesis and chemotherapy resistance. However, little is known about how USP1 regulates autophagy and its mechanism in tumor progression and drug sensitivity in PDAC. In this study, we found USP1 elevated in pancreatic cancer and USP1 expression inversely correlated with overall survival. USP1 depletion inhibited cell proliferation, epithelial-mesenchymal transition, and migration in PDAC cells. Interestingly, USP1 knockdown or inhibition reduced autophagy initi

SUBMITTER: Li L 

PROVIDER: S-EPMC11871461 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature