The NFIB/CARM1 partnership is a driver in preclinical models of small cell lung cancer

Guozhen Gao, Simone Hausmann, Natasha M. Flores, Ana Morales Benitez, Jianjun Shen, Xiaojie Yang, Maria D. Person, Sitaram Gayatri, Donghang Cheng, Yue Lu, Bin Liu, Pawel K. Mazur () and Mark T. Bedford ()
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Guozhen Gao: The University of Texas MD Anderson Cancer Center
Simone Hausmann: The University of Texas MD Anderson Cancer Center
Natasha M. Flores: The University of Texas MD Anderson Cancer Center
Ana Morales Benitez: The University of Texas MD Anderson Cancer Center
Jianjun Shen: The University of Texas MD Anderson Cancer Center
Xiaojie Yang: The University of Texas MD Anderson Cancer Center
Maria D. Person: The University of Texas at Austin
Sitaram Gayatri: The University of Texas MD Anderson Cancer Center
Donghang Cheng: The University of Texas MD Anderson Cancer Center
Yue Lu: The University of Texas MD Anderson Cancer Center
Bin Liu: The University of Texas MD Anderson Cancer Center
Pawel K. Mazur: The University of Texas MD Anderson Cancer Center
Mark T. Bedford: The University of Texas MD Anderson Cancer Center

Nature Communications, 2023, vol. 14, issue 1, 1-15

Abstract: Abstract The coactivator associated arginine methyltransferase (CARM1) promotes transcription, as its name implies. It does so by modifying histones and chromatin bound proteins. We identified nuclear factor I B (NFIB) as a CARM1 substrate and show that this transcription factor utilizes CARM1 as a coactivator. Biochemical studies reveal that tripartite motif 29 (TRIM29) is an effector molecule for methylated NFIB. Importantly, NFIB harbors both oncogenic and metastatic activities, and is often overexpressed in small cell lung cancer (SCLC). Here, we explore the possibility that CARM1 methylation of NFIB is important for its transforming activity. Using a SCLC mouse model, we show that both CARM1 and the CARM1 methylation site on NFIB are critical for the rapid onset of SCLC. Furthermore, CARM1 and methylated NFIB are responsible for maintaining similar open chromatin states in tumors. Together, these findings suggest that CARM1 might be a therapeutic target for SCLC.

Date: 2023
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DOI: 10.1038/s41467-023-35864-y

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