A YAP/FOXM1 axis mediates EMT-associated EGFR inhibitor resistance and increased expression of spindle assembly checkpoint components

Author:

Nilsson Monique B.1ORCID,Sun Huiying1ORCID,Robichaux Jacqulyne1ORCID,Pfeifer Matthias2ORCID,McDermott Ultan2ORCID,Travers Jon2,Diao Lixia3ORCID,Xi Yuanxin3,Tong Pan3,Shen Li3,Hofstad Mia1ORCID,Kawakami Masanori1,Le Xiuning1,Liu Xi1,Fan Youhong1ORCID,Poteete Alissa1ORCID,Hu Limei1,Negrao Marcelo V.1ORCID,Tran Hai1ORCID,Dmitrovsky Ethan1,Peng David1ORCID,Gibbons Don L.1ORCID,Wang Jing3ORCID,Heymach John V.1ORCID

Affiliation:

1. Departments of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

2. Oncology R&D, AstraZeneca, Cambridge, CB2 0RE, UK.

3. Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

Abstract

YAP and FOXM1 are mediators of EGFR inhibitor resistance, and spindle proteins are therapeutic targets for this multidrug-resistant phenotype.

Funder

National Institutes of Health

National Cancer Institute

LUNGevity Foundation

University of Texas MD Anderson Cancer Center

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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