ArticleCell reports. Medicine2024
An alternative splicing signature defines the basal-like phenotype and predicts worse clinical outcome in pancreatic cancer.
Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Review
- Global landscape of protein-coding and long non-coding RNA alternative splicing and regulation in the human esophageal squamous cell carcinoma.Cancer cell international · 2026Article
- Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma.Molecular oncology · 2026Article
- HnRNP C binding to invertedScience advances · 2026Article
- Mutant KRAS promotes NF-κB driven CCL20 chemokine expression in pancreatic ductal adenocarcinoma.bioRxiv : the preprint server for biology · 2026Article
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- Article
- Alternative splicing in cancer drug resistance: Mechanisms and therapeutic prospects (Review).Oncology reports · 2026Review
- Molecular arms races at the virus-host splicing interface and their pathogenic implications.Frontiers in microbiology · 2026Review
- Mutant p53 regulates reversible subtype plasticity in pancreatic cancer.Cellular and molecular life sciences : CMLS · 2025Article
- RNA-binding protein quaking: a multifunctional regulator in tumour progression.Annals of medicine · 2025Review
- Development of a consensus molecular classifier for pancreatic ductal adenocarcinoma.Genome medicine · 2025Article
- Transcriptomic analysis reveals lung cancer and subtype-specific alternative splicing biomarkers regulated by RNA-binding proteins.Molecular therapy. Nucleic acids · 2025Article
- Organoid models in oncology: advancing precision cancer therapy and vaccine development.Cancer biology & medicine · 2025Review
- The Construction of ceRNA Regulatory Network Unraveled Prognostic Biomarkers and Repositioned Drug Candidates for the Management of Pancreatic Ductal Adenocarcinoma.Current issues in molecular biology · 2025Article
- Targeting PTBP3-Mediated Alternative Splicing of COX11 Induces Cuproptosis for Inhibiting Gastric Cancer Peritoneal Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Personalized PDAC chip with functional endothelial barrier for tumour biomarker detection: A platform for precision medicine applications.Materials today. Bio · 2024Article
- Steering research on mRNA splicing in cancer towards clinical translation.Nature reviews. Cancer · 2024Review
- A single-cell strategy for the identification of intronic variants related to mis-splicing in pancreatic cancer.NAR genomics and bioinformatics · 2024Article
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Authors and funding
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is characterized by extremely poor prognosis. PDAC presents with molecularly distinct subtypes, with the basal-like one being associated with enhanced chemoresistance. Splicing dysregulation contributes to PDAC; however, its involvement in subtype specification remains elusive. Herein, we uncover a subtype-specific splicing signature associated with prognosis in PDAC and the splicing factor Quaking (QKI) as a determinant of the basal-like signature. Single-cell sequencing analyses highlight QKI as a marker of the basal-like phenotype. QKI represses splicing events associated with the classical subtype while promoting basal-like events associated with shorter survival. QKI favors a plastic, quasi-mesenchymal phenotype that supports migration and chemoresistance in PDAC organoids and cell lines, and its expression is elevated in high-grade primary tumors and metastatic lesions. These studies identify a splicing signature that defines PDAC subtypes and indicate that QKI promotes an undifferentiated, plastic phenotype, which renders PDAC cells chemoresistant and adaptable to environmental changes.
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