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Multiple roles and context-specific mechanisms underlying YAP and TAZ-mediated resistance to anti-cancer therapy

Francesca Reggiani1, Giulia Gobbi1, Alessia Ciarrocchi1

  • 1Laboratory of Translational Research, Azienda USL- IRCCS di Reggio Emilia, Reggio Emilia, Italy.

Biochimica Et Biophysica Acta. Reviews on Cancer
|January 14, 2020
PubMed

Insights

YAP/TAZ cofactors drive cancer drug resistance. Inhibiting YAP/TAZ, potentially with BET inhibitors, may overcome resistance to various cancer therapies, including immunotherapy.

Area of Science:

  • Molecular oncology
  • Cancer biology
  • Drug resistance mechanisms

Background:

  • Yeast association protein (YAP) and Tafazzin (TAZ) act as oncogenes in various cancers.
  • Dysregulated YAP/TAZ signaling contributes to resistance against chemotherapy, targeted therapy, and hormone therapy.
  • YAP/TAZ activity impacts tumor and microenvironment cells, influencing immunotherapy response.

Purpose of the Study:

  • To elucidate the role of YAP/TAZ in mediating resistance to diverse anti-cancer treatments.
  • To explore therapeutic strategies targeting YAP/TAZ to overcome drug resistance.
  • To investigate the potential of BET inhibitors in combination therapy for cancer.

Main Methods:

  • Review of molecular mechanisms underlying YAP/TAZ-mediated drug resistance.
  • Analysis of signaling pathways converging on YAP/TAZ.
  • Evaluation of compounds targeting YAP/TAZ function and expression.

Main Results:

  • YAP/TAZ deregulation is a key mechanism of resistance across multiple cancer therapy types.
  • Inhibiting YAP/TAZ function offers a potential strategy to re-sensitize tumors to treatment.
  • Simultaneous targeting of YAP/TAZ expression and activity, e.g., via BET inhibitors, shows promise.

Conclusions:

  • YAP/TAZ cofactors are critical mediators of anti-cancer drug resistance.
  • Targeting YAP/TAZ pathways represents a viable strategy to improve therapeutic outcomes.
  • BET inhibitors offer a promising approach for combined therapy by inhibiting both YAP/TAZ expression and activity.
Keywords:
Cancer therapyDrug resistanceHippoTAZYAP

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