RGC-32介导 TGF-β诱导的胰腺癌BxPC-3细胞EMT过程

IObjective To investigate the role of RGC-32 in EMT process of pancreatic cancer cell line BxPC-3. Methods To explore whether RGC-32 is controlled by TGF-β and its possible role in TGF-β-induced EMT, human pancreatic cancer cell line BxPC-3 (Smad4 homozygous deleted) was treated with TGF-β1, and the morphology of cells was visualized with a phase contrast microscope (×200, Nikon, Japan). RGC-32 siRNA silencing and gene transfection were performed as well. The expression of RGC-32 and EMT-related markers at mRNA and protein levels was determined by real-time quantitative RT-PCR and western blot respectively. Results In vitro, we found sustained TGF-β stimuli induced EMT and up-regulated RGC-32 expression in BxPC-3 cells. By means of gene over-expression and RNA interference, we further demonstrated that RGC-32 not only mediated TGF-β-induced EMT, but also induced EMT independently in BxPC-3 cells, which was independent of Smad signal pathways. Conclusions RGC-32 might be a new metastasis promoting factor for pancreatic cancer and it can enhance metastatic phenotype of pancreatic cancer cells by mediating TGF-β-induced EMT.