ArticleProceedings of the National Academy of Sciences of the United States of America2023
RNA-binding motif protein 10 inactivates c-Myc by partnering with ribosomal proteins uL18 and uL5.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Nucleolar-localized sialidase Neu4 suppresses cell proliferation through destabilizing c-Myc via interacting with ribosomal proteins L5 and L11.Glycoconjugate journal · 2026Article
- Cyclic di-GMP suppresses cancer metastasis by targeting proteasome 26S subunit non-ATPase 3 independently of STING.Signal transduction and targeted therapy · 2026Article
- SNORA47 affects stemness and chemotherapy sensitivity via EBF3/RPL11/c-Myc axis in luminal A breast cancer.Molecular medicine (Cambridge, Mass.) · 2025Article
- Deciphering the tumor-suppressive role of RBMS3 in lung adenocarcinoma through genomic insights into prognosis and mechanisms.Scientific reports · 2025Article
- Silencing RPL11 attenuates acute kidney injury by suppressing tubular apoptosis and macrophage-driven inflammation.Frontiers in immunology · 2025Article
- RBM10 Mutation as a Potential Negative Prognostic/Predictive Biomarker to Therapy in Non-Small-Cell Lung Cancer.Clinical lung cancer · 2024Article
- High-throughput transcriptome profiling indicates ribosomal RNAs to be associated with resistance to immunotherapy in non-small cell lung cancer (NSCLC).Journal for immunotherapy of cancer · 2024Article
- Multidimensional biological characteristics of ground glass nodules.Frontiers in oncology · 2024Review
- Negative Regulation of CPSF6 Suppresses the Warburg Effect and Angiogenesis Leading to Tumor Progression Via c-Myc Signaling Network: Potential Therapeutic Target for Liver Cancer Therapy.International journal of biological sciences · 2024Article
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
RNA-binding motif protein 10 (RBM10) is a frequently mutated tumor suppressor in lung adenocarcinoma (LUAD). Yet, it remains unknown whether cancer-derived mutant RBM10 compromises its tumor suppression function and, if so, the molecular insight of the underlying mechanisms. Here, we show that wild-type RBM10 suppresses lung cancer cell growth and proliferation by inactivating c-Myc that is essential for cancer cell survival. RBM10 directly binds to c-Myc and promotes c-Myc's ubiquitin-dependent degradation, while RBM10 knockdown leads to the induction of c-Myc level and activity. This negative action on c-Myc is further boosted by ribosomal proteins (RPs) uL18 (RPL5) and uL5 (RPL11) via their direct binding to RBM10. Cancer-derived mutant RBM10-I316F fails to bind to uL18 and uL5 and to inactivate c-Myc, thus incapable of suppressing tumorigenesis. Our findings uncover RBM10 as a pivotal c-Myc repressor by cooperating with uL18 and uL5 in lung cancer cells, as its failure to do so upon mutation favors tumorigenesis.
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