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YAP1-Mediated CDK6 Activation Confers Radiation Resistance in Esophageal Cancer - Rationale for the Combination of

Fan Li1,2, Yan Xu1, Bovey Liu1

  • 1Department of Gastrointestinal Medical Oncology, U.T.MD. Anderson Cancer Center, Houston, Texas.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|December 20, 2018
PubMed
Abstract

Insights

Targeting YAP1 and CDK6 pathways offers a new strategy against therapy-resistant esophageal cancer. Inhibiting both YAP1 and CDK6 overcomes radiation resistance and reduces tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • Esophageal cancer is a deadly disease with frequent resistance to therapy.
  • Alterations in YAP1 and CDK6 are common in esophageal cancer and may drive treatment resistance.

Purpose of the Study:

  • To investigate the role of YAP1 and CDK6 in esophageal cancer therapy resistance.
  • To explore the therapeutic potential of targeting YAP1 and CDK6 pathways.

Main Methods:

  • Examined YAP1 and CDK6 expression in esophageal cancer cells and tissues.
  • Investigated YAP1-mediated CDK6 activation and its link to radiation resistance.
  • Utilized pharmacologic and genetic inhibition of YAP1 and CDK6 for in vitro and in vivo studies.

Main Results:

  • YAP1 and CDK6 expression are positively correlated in resistant esophageal cancer.
  • YAP1 upregulation promotes radiation resistance; YAP1 inhibition sensitizes cells to radiation.
  • CDK6 inhibition also sensitizes cells to radiation, revealing a feed-forward loop with YAP1.
  • Combined inhibition of YAP1 and CDK6 reduced tumor growth, stem cell populations, and enhanced radiosensitivity.

Conclusions:

  • A positive crosstalk between YAP1 and CDK6 pathways contributes to esophageal cancer radiation resistance.
  • Simultaneous targeting of YAP1 and CDK6 pathways presents a promising therapeutic strategy for overcoming resistance in esophageal cancer.

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