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Updated: May 12, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

YAP/TEAD-mediated transcription controls cellular senescence

Qi Xie1, Jing Chen, Han Feng

  • 1State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.

Cancer Research
|April 12, 2013
PubMed

Insights

Yes-associated protein (YAP) regulates cellular senescence. YAP deficiency induces senescence, while its expression suppresses it, offering potential cancer therapy targets.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Yes-associated protein (YAP) is a key transcription coactivator regulating cell proliferation and apoptosis.
  • The role of YAP in cellular senescence remains largely unexplored.

Purpose of the Study:

  • To elucidate the role of YAP in regulating cellular senescence.
  • To identify downstream targets of YAP involved in senescence.
  • To explore the therapeutic potential of targeting YAP in cancer.

Main Methods:

  • Replication-induced senescence in IMR90 cells.
  • YAP silencing and ectopic expression.
  • TEAD, Rb/p16/p53 pathway analysis.
  • Cdk6 expression and functional assays.
  • Chemotherapeutic agent treatment in tumor cells.

Main Results:

  • YAP protein levels decrease during replication-induced senescence.
  • YAP silencing inhibits proliferation and induces premature senescence.
  • Senescence induced by YAP deficiency is TEAD- and Rb/p16/p53-dependent.
  • Cdk6 is a direct downstream target of YAP, mediating senescence.
  • YAP or Cdk6 expression rescues YAP knockdown-induced senescence.
  • Downregulation of YAP enhances chemotherapy-induced senescence in tumor cells.

Conclusions:

  • YAP plays a critical role in regulating cellular senescence.
  • The YAP-TEAD complex regulates Cdk6 expression, impacting senescence.
  • Targeting YAP or Cdk6 presents a potential therapeutic strategy for tumor suppression via senescence induction.

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