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The NFIB/CARM1 Partnership is a Therapeutic Target for Small Cell Lung Cancer

ABSTRACT: This project identified NFI family members as CARM1 substrates. NFIB was previously reported to play a critical role in the development of small cell lung cancer. We provided evidence that the arginine methylation of NFIB is required for its oncogenic function in small cell lung cancer.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell

DISEASE(S): Lung Small Cell Carcinoma,Cervix Carcinoma

SUBMITTER: Maria Person

LAB HEAD: Mark T. Bedford

PROVIDER: PXD038237 | Pride | 2023-02-07

REPOSITORIES: Pride

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			Action	DRS
	7289_GG_1-01.mzid.gz	Mzid
	7289_GG_1-01.mzid_7289_GG_1-01.MGF	Mzid
	7289_GG_1.raw	Raw
	7289_GG_2.mzid.gz	Mzid
	7289_GG_2.mzid_7289_GG_2.MGF	Mzid

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Publications

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

Gao Guozhen G Hausmann Simone S Flores Natasha M NM Benitez Ana Morales AM Shen Jianjun J Yang Xiaojie X Person Maria D MD Gayatri Sitaram S Cheng Donghang D Lu Yue Y Liu Bin B Mazur Pawel K PK Bedford Mark T MT

Nature communications 20230123 1

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 overexpre ...[more]

PMID: 36690626

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The NFIB/CARM1 Partnership is a Therapeutic Target for Small Cell Lung Cancer

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The NFIB/CARM1 Axis is a Therapeutic Target for Small Cell Lung Cancer

Project description:We identified NFIB as a CARM1 substrate and showed that this transcription factor utilizes CARM1 as a coactivator. Importantly, NFIB harbors both oncogenic and metastatic activities, and is often overexpressed in small cell lung cancer (SCLC). 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. By performing the high-throughput sequecing analysis, we found that CARM1-null and NFIB-R388K mutant mouse SCLC tumors share the ability to regulate chromatin accessbility and have similar gene expression pattern.

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CARM1-expressing ovarian cancer depends on the histone methyltransferase EZH2 activity [RNA-Seq]

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