CX26 promotes pancreatic cancer progression by competitively inhibiting interaction of c-Myc with PSMD2 and enhancing c-Myc stability.

ABSTRACT:

Background

Pancreatic cancer (PC) is highly aggressive and fatal and has dismal prognostic outcomes, primarily due to its late-stage diagnosis and limited effective treatments. The molecular mechanisms triggering PC progression are largely unclear. This study investigated how CX26 contributes to pancreatic cancer development and its potential as a therapeutic target.

Methods

CX26 expression in PC and its clinical significance were examined through bioinformatics analysis. The biological functions of CX26 in PC cells were explored via colony formation, CCK-8, and proteomic analysis. To explore the mechanisms by which CX26 regulates c-Myc stability, co-immunoprecipitation, immunofluorescence, and molecular docking were utilized to investigate the interactions among CX26, PSMD2

SUBMITTER: He C 

PROVIDER: S-EPMC12366093 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature