Overexpression of response gene to complement 32 (RGC32) promotes cell invasion and induces epithelial–mesenchymal transition in lung cancer cells via the NF-κB signaling pathway

详细信息    查看全文

• 作者：Qinying Sun (1)
  Xiaopeng Yao (1)
  Yunye Ning (1)
  Wei Zhang (1)
  Guowu Zhou (1)
  Yuchao Dong (1)
  
• 关键词：Response gene to complement 32 ; Lung cancer ; Invasion ; Migration ; Epithelial–mesenchymal transition ; Nuclear factor ; κB
• 刊名：Tumor Biology
• 出版年：2013
• 出版时间：October 2013
• 年：2013
• 卷：34
• 期：5
• 页码：2995-3002
• 全文大小：
• 作者单位：Qinying Sun (1)
  Xiaopeng Yao (1)
  Yunye Ning (1)
  Wei Zhang (1)
  Guowu Zhou (1)
  Yuchao Dong (1)
  
  1. Department of Respiratory Medicine, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai, 200433, People’s Republic of China
  
• ISSN：1423-0380

文摘

Response gene to complement 32 (RGC32) is a novel cellular protein that has been reported to be expressed aberrantly in multiple types of human tumors. However, the role of RGC32 in cancer is still controversial, and the molecular mechanisms by which RGC32 contributes to the development of cancer remain largely unknown. In the present study, we constructed a recombinant expression vector pCDNA3.1-RGC32 and transfected it into human lung cancer A549 cells. Stable transformanted cells were identified by real-time PCR and Western blot analysis. Functional analysis showed that forced overexpression of RGC32 increased invasive and migration capacities of lung cancer cells in vitro, and induced the acquisition of epithelial–mesenchymal transition (EMT) phenotype, as demonstrated by the spindle-like morphology, downregulation of E-cadherin, and upregulation of Vimentin, Fibronectin, Snail and Slug. Also, overexpression of RGC32 increased expression and activities of matrix metalloproteinase (MMP)-2 and MMP-9 in A549 cells. Furthermore, the downregulation of E-cadherin induced by RGC32 was remarkably attenuated by nuclear factor-κB (NF-κB) inhibitor BAY 11-7028 and small interfering RNA targeting NF-κB p65, suggesting a role of the NF-κB signaling pathway in RGC32-induced EMT. Taken together, our data suggest that RGC32 promotes cell migration and invasion and induces EMT in lung cancer cells via the NF-κB signaling pathway.