Linking cancer transcriptional addictions by CDK7 to YAP/TAZ.
Department of Molecular Medicine, University of Padua School of Medicine, 35121 Padua, Italy; IFOM, The FIRC Institute of Molecular Oncology, 35121 Padua, Italy [email protected].
- Published Article
Genes & development
- Publication Date
Jan 01, 2020
Inhibition of CDK7 is a promising strategy for cancer therapy. CDK7 so far has been understood mainly in the context of Pol II-driven transcription. However, how are the roles of CDK7 in the "basal" transcriptional machinery reconciled with the function of CDK7 as inducer of specific transcriptional programs in tumor cells? In this issue of Genes & Development, Cho and colleagues (pp. 53-71) advance in this direction, demonstrating that attenuation of CDK7 fosters the oncogenic activity of the YAP/TAZ/Yki coactivators. CDK7 directly phosphorylates YAP/TAZ/Yki in the nucleus, protecting them from ubiquitination and degradation, in a manner independent from the Hippo cascade and independent from CDK7 basal transcriptional functions. © 2020 Piccolo; Published by Cold Spring Harbor Laboratory Press.
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The corresponding record at NLM can be accessed at https://www.ncbi.nlm.nih.gov/pubmed/31896688