ArticlePLoS genetics2014
The RNA-binding protein QKI suppresses cancer-associated aberrant splicing.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
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Who cites it
161 citing papers in PubMed, 251 citations in OpenAlex.
- RAISE quantifies RNA binding protein activity via transcriptomic profiling.Nature communications · 2026Article
- The Role of Alternative Splicing in Lung Cancer: Mechanisms, Regulators, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Tumoral switch in NUMB splicing changes essential transcription pathways and induces malignant properties in tumour cells.Genome biology · 2026Article
- Article
- Competition for the conserved branch point sequence influences physiological outcomes in pre-mRNA splicing.eLife · 2026Article
- The identification of RNA splicing aberrations and their potential regulatory network in Chinese non-small cell lung cancer.Respiratory research · 2026Article
- Mechanistic insights and clinical implications of RNA-binding proteins in prostate cancer.Discover oncology · 2026Review
- Alternative splicing events show high prognostic values and indicate potential core genes in acute myeloid leukemia.Clinical and experimental medicine · 2026Article
- RNA-Binding Proteins in Adipose Biology: From Mechanistic Understanding to Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Synergistic amelioration of cholestatic liver fibrosis by combined total astragalus saponins and AAV8.Frontiers in pharmacology · 2026Article
- RNA-binding protein quaking: a multifunctional regulator in tumour progression.Annals of medicine · 2025Review
- APDCA: An accurate and effective method for predicting associations between RBPs and AS-events during epithelial-mesenchymal transition.PLoS computational biology · 2025Article
- SNRPB promotes gastric cancer progression by regulating aberrant splicing of PUF60.Cell death & disease · 2025Article
- Transcriptomic analysis reveals lung cancer and subtype-specific alternative splicing biomarkers regulated by RNA-binding proteins.Molecular therapy. Nucleic acids · 2025Article
- QKI ensures splicing fidelity during cardiogenesis by engaging the U6 tri-snRNP to activate splicing at weak 5' splice sites.bioRxiv : the preprint server for biology · 2025Article
- Upregulation of YY1 in M2 macrophages promotes secretion of exosomes containing hsa-circ-0000326 via super-enhancers to facilitate prostate cancer progression.Molecular and cellular biochemistry · 2025Article
- Loss of DDX24 inhibits lung cancer progression by stimulating IKBKG splicing-mediated autophagy.Theranostics · 2025Article
- The canonical Wnt pathway in osteoporosis: a scoping review of key compounds and proteins modulating Wnt-induced osteogenesis.Frontiers in pharmacology · 2025Review
- Qki5 safeguards spinal motor neuron function by defining the motor neuron-specific transcriptome via pre-mRNA processing.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Transcriptomic Alterations in Spliceosome Components in Advanced Heart Failure: Status of Cardiac-Specific Alternative Splicing Factors.International journal of molecular sciences · 2024Article
101 more citing papers are in PubMed but not listed here.
Corrections and comments
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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
Lung cancer is the leading cause of cancer-related death worldwide. Aberrant splicing has been implicated in lung tumorigenesis. However, the functional links between splicing regulation and lung cancer are not well understood. Here we identify the RNA-binding protein QKI as a key regulator of alternative splicing in lung cancer. We show that QKI is frequently down-regulated in lung cancer, and its down-regulation is significantly associated with a poorer prognosis. QKI-5 inhibits the proliferation and transformation of lung cancer cells both in vitro and in vivo. Our results demonstrate that QKI-5 regulates the alternative splicing of NUMB via binding to two RNA elements in its pre-mRNA, which in turn suppresses cell proliferation and prevents the activation of the Notch signaling pathway. We further show that QKI-5 inhibits splicing by selectively competing with a core splicing factor SF1 for binding to the branchpoint sequence. Taken together, our data reveal QKI as a critical regulator of splicing in lung cancer and suggest a novel tumor suppression mechanism involving QKI-mediated regulation of the Notch signaling pathway.
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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.