Bax Downregulation Suppresses Mitochondrial Apoptosis and Promotes Tumor Progression

Review Article

Abstract

Pediatric gastrointestinal tumors (PGITs) exhibit defective mitochondrial apoptosis, but Bax’s role remains unclear. This study explored Bax function in PGITs via in vitro assays. Bax was downregulated in PGIT cell lines (HT-29, WiDr, Caco-2) vs. normal HIEC-6. Bax overexpression promoted mitochondrial apoptosis, activated Caspase cascade, and inhibited proliferation, identifying Bax as a potential PGIT therapeutic target.