YAP and TAZ: Monocorial and bicorial transcriptional co-activators in human cancers
Federica Lo Sardo1, Valeria Canu1, Marcello Maugeri-Saccà2
1Translational Oncology Research Unit, Department of Research, Diagnosis and Innovative Technologies, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Abstract:
The transcriptional regulators YAP and TAZ are involved in numerous physiological processes including organ development, growth, immunity and tissue regeneration. YAP and TAZ dysregulation also contribute to tumorigenesis, thereby making them attractive cancer therapeutic targets. Arbitrarily, YAP and TAZ are often considered as a single protein, and are referred to as YAP/TAZ in most studies. However, increasing experimental evidences documented that YAP and TAZ perform both overlapping and distinct functions in several physiological and pathological processes. In addition to regulating distinct processes, YAP and TAZ are also regulated by distinct upstream cues. The aim of the review is to describe the distinct roles of YAP and TAZ focusing particularly on cancer. Therapeutic strategies targeting either YAP and TAZ proteins or only one of them should be carefully evaluated. Selective targeting of YAP or TAZ may in fact impair different pathways and determine diverse clinical outputs.
Insights
The transcriptional regulators YAP and TAZ have distinct roles in health and cancer. Understanding these differences is crucial for developing targeted cancer therapies that selectively inhibit YAP or TAZ.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- The transcriptional regulators YAP (Yes-associated protein) and TAZ (Tazo) are key players in cellular processes.
- Dysregulation of YAP and TAZ is implicated in cancer development.
- YAP and TAZ are often studied together as YAP/TAZ, but possess unique functions.
Purpose of the Study:
- To review the distinct roles of YAP and TAZ, with a focus on their involvement in cancer.
- To highlight the importance of differentiating YAP and TAZ functions for therapeutic strategies.
- To emphasize the need for careful evaluation of targeted therapies against YAP or TAZ.
Main Methods:
- Literature review of experimental evidence on YAP and TAZ functions.
- Analysis of distinct upstream regulatory cues for YAP and TAZ.
- Examination of the implications of YAP and TAZ dysregulation in tumorigenesis.
Main Results:
- YAP and TAZ regulate both overlapping and distinct physiological and pathological processes.
- Distinct upstream signals control YAP and TAZ activity.
- Targeting YAP or TAZ selectively may impact different pathways, leading to varied clinical outcomes.
Conclusions:
- YAP and TAZ are not interchangeable and exhibit unique functions.
- Therapeutic strategies targeting YAP and TAZ require careful consideration of their individual roles.
- Selective inhibition of YAP or TAZ could offer distinct therapeutic benefits or challenges in cancer treatment.
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