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SIRT1 regulates YAP2-mediated cell proliferation and chemoresistance in hepatocellular carcinoma

B Mao1, F Hu2, J Cheng1

  • 1Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.

Oncogene
|April 2, 2013
PubMed

Insights

SIRT1 deacetylates YAP2, promoting hepatocellular carcinoma (HCC) cell growth and cisplatin resistance. Targeting SIRT1 may offer new therapeutic strategies for HCC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The mammalian Ste20-like kinase/Yes-associated protein 2 (MST/YAP) pathway is crucial in hepatocellular carcinoma (HCC) development.
  • YAP2 activity is regulated by phosphorylation and dephosphorylation, but its acetylation remains largely uncharacterized.

Purpose of the Study:

  • To investigate the role of SIRT1 in regulating YAP2 acetylation and its impact on HCC progression and drug resistance.

Main Methods:

  • Analysis of SIRT1 expression in HCC patient tumor samples.
  • In vitro experiments using HCC cells to assess SIRT1-mediated YAP2 deacetylation.
  • Investigating the effect of SIRT1 on YAP2/TEAD4 interaction and transcriptional activity.
  • Evaluating the impact of SIRT1 knockdown on cisplatin (CDDP)-induced YAP2 nuclear translocation and chemosensitivity.

Main Results:

  • SIRT1 expression is upregulated in HCC tumors and correlates with connective tissue growth factor (CTGF) levels.
  • SIRT1 deacetylates YAP2 in HCC cells, enhancing YAP2/TEAD4 association and promoting cell growth.
  • SIRT1 knockdown inhibits CDDP-induced YAP2 nuclear translocation and increases HCC cell sensitivity to CDDP.

Conclusions:

  • SIRT1-mediated deacetylation of YAP2 represents a novel regulatory mechanism in HCC tumorigenesis.
  • This pathway influences HCC cell growth and resistance to chemotherapy, suggesting SIRT1 as a potential therapeutic target.

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