Senesce to Survive: YAP-Mediated Dormancy Escapes EGFR/MEK Inhibition

Igor Bado; Xiang H-F Zhang

doi:10.1016/j.ccell.2019.12.008

Senesce to Survive: YAP-Mediated Dormancy Escapes EGFR/MEK Inhibition

Cancer Cell. 2020 Jan 13;37(1):1-2. doi: 10.1016/j.ccell.2019.12.008.

Authors

Igor Bado¹, Xiang H-F Zhang²

Affiliations

¹ Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Dan L. Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
² Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Dan L. Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; McNair Medical Institute, Baylor College of Medicine, BCM600, One Baylor Plaza, Houston, TX 77030, USA. Electronic address: xiangz@bcm.edu.

PMID: 31951560
DOI: 10.1016/j.ccell.2019.12.008

Abstract

Therapeutic resistance is a major challenge in cancer treatment. In this issue of Cancer Cell, Kurppa et al. demonstrated that a senescence-like state enables lung cancer cells to survive dual inhibition of EGFR and MEK. This was mediated by the YAP/TEAD pathway, which drives epigenomic reprogramming and EMT to counteract apoptosis.

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MeSH terms

Adaptor Proteins, Signal Transducing
Drug Resistance, Neoplasm / drug effects*
ErbB Receptors
Protein Kinase Inhibitors*
Transcription Factors

Substances

Adaptor Proteins, Signal Transducing
Protein Kinase Inhibitors
Transcription Factors
ErbB Receptors