Bcl-2 Overexpression Inhibits Mitochondrial Apoptosis and Promotes Tumor Progression

Review Article

Abstract

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