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SENP2 Regulates Hepatocellular Carcinoma Cell Growth by Modulating the Stability of β-catenin

  • Shen, Huo-Jian (Department of General Surgery, Renji hospital of Shanghai Jiao Tong University School of Medicine) ;
  • Zhu, Hong-Yi (Department of General Surgery, Renji hospital of Shanghai Jiao Tong University School of Medicine) ;
  • Yang, Chao (Department of General Surgery, Renji hospital of Shanghai Jiao Tong University School of Medicine) ;
  • Ji, Fu (Department of General Surgery, Renji hospital of Shanghai Jiao Tong University School of Medicine)
  • Published : 2012.08.31

Abstract

SUMOylation has emerged as an important post-translational modification that modulates the localization, stability and activity of a broad spectrum of proteins. A dynamic process, it can be reversed by a family of SUMO-specific proteases (SENPs). However, the biological roles of SENPs in mammalian development and pathogenesis remain largely elusive. Here, we demonstrated that SENP2 plays a critical role in the control of hepatocellular carcinoma cell growth. SENP2 was found to be down-regulated in hepatocellular carcinoma (HCC) tissues and over-expression suppressed the growth and colony formation of HCC cells. In contrast, silencing of SENP2 by siRNAs promoted cancer cell growth. We further found that stability of ${\beta}$-catenin was markedly decreased when SENP2 was over-expressed. Interestingly, the decrease was dependent on the de-SUMOylation activity of SENP2, because over-expression of a SENP2 catalytic mutant form had no obviously effects on ${\beta}$-catenin. Our results suggest that SENP2 might play a role in hepatocellular carcinoma cell growth control by modulating the stability of ${\beta}$-catenin.

Keywords

References

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