Prohibitin Induces Apoptosis in BGC823 Gastric Cancer Cells Through the Mitochondrial Pathway

Abstract

Prohibitin (PHB), an evolutionarily-conserved protein, has been found to be over-expressed in gastriccancer and be closely related with tumor malignancy. In this study, to investigate the relationship between PHBexpression and cell apoptosis in the BGC823 gastric cancer cell line, low and high expression PHB in BGC823cells was accomplished using RNA interference technology and gene transfer techniques. Cell proliferation, cellcycling, apoptosis, Bax, Bcl-2 and Cyt.c protein expression and the activation of Caspase-3,9 were assessed after48h. Over-expression of PHB gene in BGC823 cells resulted in slow cell growth, cell arrest in G2 phase, and anincreased apoptosis ratio while the opposite was found for PHB under-expressing cells. In PHB over-expressingcells, the expression of Bax gene was increased, the expression of Bcl-2 was decreased, the activation level ofCaspase-3, 9 was increased, but the activation level of Caspase-8 demonstrated no change. These results indicatethat PHB induced apoptosis through the mitochondrial pathway.