ArticleScientific reports2017
Functional analysis reveals that RBM10 mutations contribute to lung adenocarcinoma pathogenesis by deregulating splicing.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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63 citing papers in PubMed, 97 citations in OpenAlex.
- Genomic Characterization of Lung Cancer in Never-Smokers Using Deep Learning.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2026Article
- RBM10 modulation of circRNA biogenesis contributes to its tumor suppressor role in lung adenocarcinoma.Biomarker research · 2026Article
- Article
- Splicing Shift of RAC1 Accelerates Tumorigenesis and Defines a Potent Therapeutic Target in Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- HIV-1 Vpu interacts with RBM10 to promote HIV-1 infection.mSystems · 2025Article
- RBM10 loss promotes metastases by aberrant splicing of cytoskeletal and extracellular matrix mRNAs.The Journal of experimental medicine · 2025Article
- Expression pattern, immune signature, and prognostic value of RBM10 in human cancers.Histology and histopathology · 2025Article
- RBM10 inhibits pancreatic cancer development by suppressing immune escape through PD-1 expression.Journal of Cancer · 2025Article
- ZC3H18 regulates alternative splicing and related genes in cervical cancer.Frontiers in genetics · 2025Article
- Integrating Bulk RNA and Single-Cell RNA Sequencing Identifies and Validates Lactylation-Related Signatures for Intervertebral Disc Degeneration.Journal of cellular and molecular medicine · 2024Article
- RBM10 Mutation as a Potential Negative Prognostic/Predictive Biomarker to Therapy in Non-Small-Cell Lung Cancer.Clinical lung cancer · 2024Article
- Splicing regulation through biomolecular condensates and membraneless organelles.Nature reviews. Molecular cell biology · 2024Review
- Harnessing DNA replication stress to target RBM10 deficiency in lung adenocarcinoma.Nature communications · 2024Article
- RBM10 loss induces aberrant splicing of cytoskeletal and extracellular matrix mRNAs and promotes metastatic fitness.bioRxiv : the preprint server for biology · 2024Article
- Investigation ofHeliyon · 2024Article
- The splicing regulators RBM5 and RBM10 are subunits of the U2 snRNP engaged with intron branch sites on chromatin.Molecular cell · 2024Article
- RBM10 C761Y mutation induced oncogenic ASPM isoforms and regulated β-catenin signaling in cholangiocarcinoma.Journal of experimental & clinical cancer research : CR · 2024Article
- Targeting dysregulated splicing factors in cancer: lessons learned from RBM10 deficiency.Journal of molecular cell biology · 2024Article
- Alternative splicing and related RNA binding proteins in human health and disease.Signal transduction and targeted therapy · 2024Review
- RNA-binding motif protein 10 inactivates c-Myc by partnering with ribosomal proteins uL18 and uL5.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RBM10 is an RNA splicing regulator that is frequently mutated in lung adenocarcinoma (LUAD) and has recently been proposed to be a cancer gene. How RBM10 mutations observed in LUAD affect its normal functions, however, remains largely unknown. Here integrative analysis of RBM10 mutation and RNA expression data revealed that LUAD-associated RBM10 mutations exhibit a mutational spectrum similar to that of tumor suppressor genes. In addition, this analysis showed that RBM10 mutations identified in LUAD patients lacking canonical oncogenes are associated with significantly reduced RBM10 expression. To systematically investigate RBM10 mutations, we developed an experimental pipeline for elucidating their functional effects. Among six representative LUAD-associated RBM10 mutations, one nonsense and one frameshift mutation caused loss-of-function as expected, whereas four missense mutations differentially affected RBM10-mediated splicing. Importantly, changes in proliferation rates of LUAD-derived cells caused by these RBM10 missense mutants correlated with alterations in RNA splicing of RBM10 target genes. Together, our data implies that RBM10 mutations contribute to LUAD pathogenesis, at least in large part, by deregulating splicing. The methods described in this study should be useful for analyzing mutations in additional cancer-associated RNA splicing regulators.
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