ACLY Overexpression Drives Lipid Metabolic Reprogramming and Tumor Progression

Review Article

Abstract

Pediatric gastrointestinal tumors (PGITs) rely on abnormal lipid metabolism for growth, but ACLY’s role remains unclear. This study explored ACLY function in PGITs via in vitro assays. ACLY was overexpressed in PGIT cell lines (HT-29, WiDr, Caco-2) vs. normal HIEC-6. ACLY silencing reduced lipid synthesis, inhibited proliferation/invasion, and activated AMPK/mTOR signaling, identifying ACLY as a potential PGIT therapeutic target.