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

Author

Listed:
  • 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
    Evozyne Inc.)

  • 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)

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.

Suggested Citation

  • 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 & Mark T., 2023. "The NFIB/CARM1 partnership is a driver in preclinical models of small cell lung cancer," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-35864-y
    DOI: 10.1038/s41467-023-35864-y
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    References listed on IDEAS

    as
    1. Evgenia Shishkova & Hao Zeng & Fabao Liu & Nicholas W. Kwiecien & Alexander S. Hebert & Joshua J. Coon & Wei Xu, 2017. "Global mapping of CARM1 substrates defines enzyme specificity and substrate recognition," Nature Communications, Nature, vol. 8(1), pages 1-13, August.
    2. Yasushi Masuda & Hidehisa Takahashi & Shigeo Sato & Chieri Tomomori-Sato & Anita Saraf & Michael P. Washburn & Laurence Florens & Ronald C. Conaway & Joan W. Conaway & Shigetsugu Hatakeyama, 2015. "TRIM29 regulates the assembly of DNA repair proteins into damaged chromatin," Nature Communications, Nature, vol. 6(1), pages 1-13, November.
    3. Young Suk Yu & Hijai R. Shin & Dongha Kim & Seon Ah Baek & Seon Ah Choi & Hyejin Ahn & Amen Shamim & Jeonghwan Kim & Ik Soo Kim & Kyeong Kyu Kim & Kyoung-Jae Won & Sung Hee Baek, 2020. "Pontin arginine methylation by CARM1 is crucial for epigenetic regulation of autophagy," Nature Communications, Nature, vol. 11(1), pages 1-18, December.
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