Response gene to complement-32 enhances metastatic phenotype by mediating transforming growth factor beta-induced epithelial-mesenchymal transition in human pancreatic cancer cell line BxPC-3

Background: response gene to complement-32 (rgc-32) is comprehensively expressed in many kinds of tissues and has been reported to be expressed abnormally in different kinds of human tumors. however,the role of rgc-32 in cancer remains controversial and no reports have described the effect of rgc-32 in pancreatic cancer. the present study investigated the expression of rgc-32 in pancreatic cancer tissues and explored the role of rgc-32 in transforming growth factor-beta (tgf-β)-induced epithelial-mesenchymal transition (emt) in human pancreatic cancer cell line bxpc-3. methods. immunohistochemical staining of rgc-32 and e-cadherin was performed on specimens from 42 patients with pancreatic cancer,12 with chronic pancreatitis and 8 with normal pancreas. to evaluate the role of rgc-32 in tgf -β induced emt in pancreatic cancer cells,bxpc-3 cells were treated with tgf-β1,and rgc-32 sirna silencing and gene overexpression were performed as well. the mrna expression and protein expression of rgc-32 and emt markers such e-cadherin and vimentin were determined by quantitative reverse transcription-pcr (qrt-pcr) and western blot respectively. finally,migration ability of bxpc-3 cells treated with tgf-β and rgc-32 sirna transfection was examined by transwell cell migration assay. results: we found stronger expression of rgc-32 and higher abnormal expression rate of e-cadherin in pancreatic cancer tissues than those in chronic pancreatitis tissues and normal pancreatic tissues. immunohistochemical analysis revealed that both rgc-32 positive expression and e-cadherin abnormal expression in pancreatic cancer were correlated with lymph node metastasis and tnm staging. in addition,a significant and positive correlation was found between positive expression of rgc-32 and abnormal expression of e-cadherin. furthermore,in vitro,we found sustained tgf-β stimuli induced emt and up-regulated rgc-32 expression in bxpc-3 cells. by means of sirna silencing and gene overexpression,we further demonstrated that rgc-32 mediated tgf -β induced emt and migration in bxpc-3 cells. conclusions: the results above indicated that rgc-32 might be a novel metastasis promoting gene in pancreatic cancer and it enhances metastatic phenotype by mediating tgf -β induced emt in human pancreatic cancer cell line bxpc-3. © 2012 zhu et al; licensee biomed central ltd.