ArticleNature communications2021
Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Outcomes Stratification of Head and Neck Cancer Using Pre- and Post-treatment DNA Methylation From Peripheral Blood.International journal of radiation oncology, biology, physics · 2023Trial
- Review
- Alternative splicing of KRAS exon 4 promotes tumor progression via enhanced KRAS4A oncogenic activity.Animal cells and systems · 2026Article
- Systematic characterization of full-length RNA isoforms in human colorectal cancer at single-cell resolution.Protein & cell · 2025Article
- Transcriptomic analysis reveals lung cancer and subtype-specific alternative splicing biomarkers regulated by RNA-binding proteins.Molecular therapy. Nucleic acids · 2025Article
- KRAS4B is required for placental development.Cellular and molecular life sciences : CMLS · 2025Article
- Alternative Splicing in Tumorigenesis and Cancer Therapy.Biomolecules · 2025Review
- Targeting the RBM39-MEK5 axis synergizes with bortezomib to inhibit the malignant growth of multiple myeloma.Blood advances · 2025Article
- Review
- The RBM39 degrader indisulam inhibits acute megakaryoblastic leukemia by altering the alternative splicing of ZMYND8.Cell & bioscience · 2025Article
- RNA-binding motif protein RBM39 enhances the proliferation of gastric cancer cells by facilitating an oncogenic splicing switch in MRPL33.Acta pharmacologica Sinica · 2025Article
- Targeting RBM39 suppresses tumor growth and sensitizes osteosarcoma cells to cisplatin.Oncogene · 2025Article
- Targeting RNA splicing modulation: new perspectives for anticancer strategy?Journal of experimental & clinical cancer research : CR · 2025Review
- Targeting KRAS: from metabolic regulation to cancer treatment.Molecular cancer · 2025Review
- Recent advances in anticancer mechanisms of molecular glue degraders: focus on RBM39-dgrading synthetic sulfonamide such as indisulam, E7820, tasisulam, and chloroquinoxaline sulfonamide.Genes & genomics · 2024Review
- IsopretGO-analysing and visualizing the functional consequences of differential splicing.NAR genomics and bioinformatics · 2024Article
- In silico RNA isoform screening to identify potential cancer driver exons with therapeutic applications.Nature communications · 2024Article
- A molecular glue RBM39-degrader induces synthetic lethality in cancer cells with homologous recombination repair deficiency.NPJ precision oncology · 2024Article
- Comparative analysis of KRAS4a and KRAS4b splice variants reveals distinctive structural and functional properties.Science advances · 2024Article
- Stem Cell Theory of Cancer: Clinical Implications for Cellular Metabolism and Anti-Cancer Metabolomics.Cancers · 2024Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
The commonly mutated human KRAS oncogene encodes two distinct KRAS4A and KRAS4B proteins generated by differential splicing. We demonstrate here that coordinated regulation of both isoforms through control of splicing is essential for development of Kras mutant tumors. The minor KRAS4A isoform is enriched in cancer stem-like cells, where it responds to hypoxia, while the major KRAS4B is induced by ER stress. KRAS4A splicing is controlled by the DCAF15/RBM39 pathway, and deletion of KRAS4A or pharmacological inhibition of RBM39 using Indisulam leads to inhibition of cancer stem cells. Our data identify existing clinical drugs that target KRAS4A splicing, and suggest that levels of the minor KRAS4A isoform in human tumors can be a biomarker of sensitivity to some existing cancer therapeutics.
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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.