PSMD14 drives lung adenocarcinoma progression through HMMR stabilization and dual activation of TGF-β/Smad and PI3K/AKT/mTOR signaling.

ABSTRACT:

Background

Lung adenocarcinoma (LUAD) represents a major subtype of non-small cell lung cancer with limited therapeutic options. While the ubiquitin-proteasome system has been implicated in cancer pathogenesis, the specific role of deubiquitinating enzymes in LUAD remains incompletely understood. This study investigates the clinical significance and molecular mechanisms of PSMD14, a crucial proteasome subunit, in LUAD progression.

Methods

We analyzed PSMD14 expression patterns across multiple databases including TCGA, GEO, and CPTAC. Functional characterization was performed through in vitro and in vivo experiments including CCK-8, colony formation, Transwell, and xenograft assays. Molecular mechanisms were elucidated using co-immunoprecipitation, ubiquitinatio

SUBMITTER: Chen R 

PROVIDER: S-EPMC12757429 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature