ArticleNature communications2023
The NFIB/CARM1 partnership is a driver in preclinical models of small cell lung cancer.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Depletion of CARM1 slows in vivo tumorigenicity and rewires developmental programming in glioma stem-like cells.Cell reports · 2026Article
- Phase Separation of NFIB Suppresses SLC3A2-Mediated Ferroptosis in Castration-Resistant Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Context-specific applications of CARM1 inhibitors: functional profiles of EZM2302 and TP-064.Molecular medicine (Cambridge, Mass.) · 2025Article
- Multifaceted roles of CARM1 beyond histone arginine methylation.Experimental & molecular medicine · 2025Review
- Identification of novel interacting proteins of FUZ and GPR161.bioRxiv : the preprint server for biology · 2025Article
- Identification of multiple genomic alterations and prediction of neoantigens from circulating tumor cells at the single-cell level.Nature communications · 2025Article
- BRD9 functions as a methylarginine reader to regulate AKT-EZH2 signaling.Science advances · 2025Article
- Loss of CARM1 alters the developmental programming of Glioma stem-like cells and creates a druggable NGFR/NTRK dependency.bioRxiv : the preprint server for biology · 2025Article
- PSMD14-mediated deubiquitination of CARM1 facilitates the proliferation and metastasis of hepatocellular carcinoma by inducing the transcriptional activation of FERMT1.Cell death & disease · 2025Article
- Sequestration of ribosomal subunits as inactive 80S by targeting eIF6 limits mitotic exit and cancer progression.Nucleic acids research · 2025Article
- PRMT3 and CARM1: Emerging Epigenetic Targets in Cancer.Journal of cellular and molecular medicine · 2025Review
- Increased nuclear factor I-mediated chromatin access drives transition to androgen receptor splice variant dependence in prostate cancer.Cell reports · 2025Article
- Roles of the NFI/CTF gene family in transcription and development: update 2025.Academia biology · 2025Article
- PIN1 is a novel interaction partner and a negative upstream regulator of the transcription factor NFIB.FEBS letters · 2024Article
- Arginine methylation-dependent TRIM47 stability mediated by CARM1 promotes the metastasis of hepatocellular carcinoma.Cell death discovery · 2024Article
- Activating Invasion and Metastasis in Small Cell Lung Cancer: Role of the Tumour Immune Microenvironment and Mechanisms of Vasculogenesis, Epithelial-Mesenchymal Transition, Cell Migration, and Organ Tropism.Cancer reports (Hoboken, N.J.) · 2024Review
- The emerging role of CARM1 in cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Small Cell Lung Cancer Neuronal Features and Their Implications for Tumor Progression, Metastasis, and Therapy.Molecular cancer research : MCR · 2024Review
- SART3 reads methylarginine-marked glycine- and arginine-rich motifs.Cell reports · 2024Article
- Protein Arginine Methyltransferase CARM1 in Human Breast Cancer.Endocrinology · 2024Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.