Bmi-1 Promotes Pancreas Tumorigenesis Via Inhibiting Ink4a-arf Locus Expression

Objective: To establish the effect knocking down Bmi-1 bring to pancreatic cancer cells for gene therapy of pancreatic cancerMethods: Construction of antisense Bmi-1 vector transfected into human pancreatic cancer PANC-1. using MTT, fluorescence microscopy observation, Western-Blot techniques to assay results; using flow cytometry to study cell cycle and apoptosis ; RT-PCR was used to study P16INK4A expression; the promoter methylation changes of P16INK4A. was demonstrated by methylation-specific PCRResults: (1) successfully constructed antisense Bmi-1 vector and high transfection efficiency. (2) transfected cell cycle arrest, apoptosis increased significantly. (3) the P16INK4A expression of transfected cells increased and the promoter methylation of its declined.Conclusions: Bmi-1 could serve as targets for gene therapy of pancreatic cancer, the expression of P16INK4A may be affected by Bmi-1 via promoting the promoter methylation of P16INK4A.