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Updated: Jan 23, 2026

De Novo Generation of Somatic Stem Cells by YAP/TAZ
Published on: May 7, 2018
YAP/TAZ Signaling and Resistance to Cancer Therapy
Chan D K Nguyen1, Chunling Yi1
1Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Abstract:
Drug resistance is a major challenge in cancer treatment. Emerging evidence indicates that deregulation of YAP/TAZ signaling may be a major mechanism of intrinsic and acquired resistance to various targeted and chemotherapies. Moreover, YAP/TAZ-mediated expression of PD-L1 and multiple cytokines is pivotal for tumor immune evasion. While direct inhibitors of YAP/TAZ are still under development, FDA-approved drugs that indirectly block YAP/TAZ activation or critical downstream targets of YAP/TAZ have shown promise in the clinic in reducing therapy resistance. Finally, BET inhibitors, which reportedly block YAP/TAZ-mediated transcription, present another potential venue to overcome YAP/TAZ-induced drug resistance.
Insights
Drug resistance in cancer may be driven by YAP/TAZ signaling. Targeting YAP/TAZ or its downstream effects with existing or novel therapies, like BET inhibitors, shows promise for overcoming treatment resistance.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Drug resistance is a significant obstacle in cancer therapy.
- YAP/TAZ signaling pathway deregulation is increasingly recognized as a key mechanism for both intrinsic and acquired resistance to various cancer treatments.
- YAP/TAZ also plays a crucial role in tumor immune evasion by promoting PD-L1 and cytokine expression.
Purpose of the Study:
- To review the role of YAP/TAZ signaling in cancer drug resistance.
- To explore therapeutic strategies targeting YAP/TAZ to overcome resistance.
- To highlight the potential of FDA-approved drugs and BET inhibitors in this context.
Main Methods:
- Literature review and synthesis of emerging evidence on YAP/TAZ signaling in cancer drug resistance.
- Analysis of therapeutic approaches targeting YAP/TAZ pathways.
- Evaluation of clinical and preclinical data on drugs affecting YAP/TAZ.
Main Results:
- YAP/TAZ pathway dysregulation contributes significantly to resistance against chemotherapy and targeted therapies.
- YAP/TAZ-driven PD-L1 and cytokine expression facilitates tumor immune evasion.
- Indirect YAP/TAZ inhibition via FDA-approved drugs and BET inhibitors demonstrates potential in preclinical and clinical settings.
Conclusions:
- YAP/TAZ signaling is a critical mediator of cancer drug resistance and immune evasion.
- Targeting YAP/TAZ, directly or indirectly, offers a promising strategy to improve therapeutic efficacy.
- Further investigation into YAP/TAZ inhibitors and combination therapies is warranted to overcome treatment resistance.
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