Asian Pacific Journal of Cancer Prevention

Asian Pacific Journal of Cancer Prevention (아시아태평양암예방학회)
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Targeting SHCBP1 Inhibits Cell Proliferation in Human Hepatocellular Carcinoma Cells

  • Tao, Han-Chuan (Department of Hepatobiliary Surgery, Wuxi Municipal People's Hospital of Nanjing Medical University) ;
  • Wang, Hai-Xiao (Department of General Surgery, Huai'an First People's Hospital of Nanjing Medical University) ;
  • Dai, Min (Department of Hepatobiliary Surgery, Wuxi Municipal People's Hospital of Nanjing Medical University) ;
  • Gu, Cheng-Yu (Department of Hepatobiliary Surgery, Wuxi Municipal People's Hospital of Nanjing Medical University) ;
  • Wang, Qun (Chinese National Human Genome Center, Rui-Jin Hospital, Shanghai Jiaotong University School of Medicine) ;
  • Han, Ze-Guang (Chinese National Human Genome Center, Rui-Jin Hospital, Shanghai Jiaotong University School of Medicine) ;
  • Cai, Bing (Department of Hepatobiliary Surgery, Wuxi Municipal People's Hospital of Nanjing Medical University)
  • Published : 2013.10.30
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Abstract

Src homology 2 domain containing (SHC) is a proto-oncogene which mediates cell proliferation and carcinogenesis in human carcinomas. Here, the SHC SH2-domain binding protein 1 (SHCBP1) was first established to be up-regulated in human hepatocellular carcinoma (HCC) tissues by array-base comparative genome hybridization (aCGH). Meanwhile, we examine and verify it by quantitative real-time PCR and western blot. Our current data show that SHCBP1 was up-regulated in HCC tissues. Overexpression of SHCBP1 could significantly promote HCC cell proliferation, survival and colony formation in HCC cell lines. Furthermore, knockdown of SHCBP1 induced cell cycle delay and suppressed cell proliferation. Furthermore, SHCBP1 could regulate the expression of activate extracellular signal-regulated kinase 1/2 (ERK1/2) and cyclin D1. Together, our findings indicate that SHCBP1 may contribute to human hepatocellular carcinoma by promoting cell proliferation and may serve as a molecular target of cancer therapy.

Keywords

References

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