Abstract
BackgroundResponse 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.MethodsImmunohistochemical 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.ResultsWe 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.ConclusionsThe 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.
Highlights
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
The abnormal expression rate of E-cadherin was significantly increased in pancreatic cancer tissues compared with normal pancreas and chronic pancreatitis tissues, but no significant differences were found between normal pancreatic tissues and pancreatitis tissues (Table 2)
By means of immunohistochemical staining, we found for the first time that the expression of RGC-32 was up-regulated in pancreatic cancer and was correlated with lymph node metastasis and TNM staging, which suggested that RGC-32 might be a novel tumor metastasis promoting factor for pancreatic cancer
Summary
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. The role of RGC32 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-b)-induced epithelial-mesenchymal transition (EMT) in human pancreatic cancer cell line BxPC-3. Accumulating evidences have indicated that epithelialmesenchymal transition (EMT), which was originally found in embryogenesis, contributes to tumor invasion, metastatic dissemination and acquisition of therapeutic resistance [3]. During the process of EMT, epithelial cells change from their epithelial characteristics including cell-cell adhesion, apical-basal polarity and lack of motility to mesenchymal features, such as invasiveness, motility and high resistance to cell death [3]. A series of molecular events occur including down-regulation of epithelial markers such as E-cadherin and upregulation of mesenchymal markers such as N-cadherin and vimentin [4]
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