RGC-32 induces transition of pancreatic cancer to epithelial mesenchyme in vivo

Abstract

ObjectivesThis study was undertaken to investigate the induction of transition of pancreatic cancer to epithelial mesenchyme by RGC-32. MethodsPrimary human pancreatic cancer cell line BXPC-3 was transfected with lentivirus overexpressing the response gene to complement-32 gene (RGC-32) and used to induce tumor in mice. The tumor sizes were measured and the expression of cytokeratin, e-cadherin and vimentin at mRNA using real time PCR and at protein levels by Western blot. ResultsCompared with the control, mice inoculated with the cells transfected with empty vector had similar tumor size while those inoculated with the cells transfected with RGC-32 expressing virus had significantly greater tumor size. HE staining showed that tumors were formed in all treatments. Molecular analyses showed that there was no difference in the expression of the cytokeratin, e-cadherin and vimentin genes at mRNA and protein levels between control and empty vector groups. However, mice derived from cells transfected with RGC-32 expressing virus had reduced cytokeratin and e-cadherin expression and increased vimentin expression. ConclusionsThese data suggest that RGC-32 promotes the proliferation of pancreatic cancer and induces the epithelial–mesenchymal transition (EMT). It would be a future direction of research to investigate the regulatory mechanism of signal molecules downstream RGC-32 on EMT-related transcription factors and deliberate the role of RGC-32 in tumorigenicity. As a result, RGC-32 may become a new therapeutic target for cancers.