ArticleFrontiers in oncology2023
MUC16 and TP53 family co-regulate tumor-stromal heterogeneity in pancreatic adenocarcinoma.
Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Characterizing the salivary RNA landscape to identify potential diagnostic, prognostic, and follow-up biomarkers for breast cancer.Molecular oncology · 2026Article
- Prognosis conferred by molecular features of appendix-derived Pseudomyxoma Peritonei.Translational oncology · 2025Article
- Leveraging Single-Cell Multi-Omics to Decode Tumor Microenvironment Diversity and Therapeutic Resistance.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Predicting Survival Signature of Bladder Cancer Related to Cancer-Associated Fibroblast (CAF) Constructed by Intersecting Genes in TCGA and GEO.Molecular biotechnology · 2024Article
- Combination of mutations in genes controlling DNA repair and high mutational load plays a prognostic role in pancreatic ductal adenocarcinoma (PDAC): a retrospective real-life study in Sardinian population.Journal of translational medicine · 2024Article
- MUC1 and MUC16: critical for immune modulation in cancer therapeutics.Frontiers in immunology · 2024Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
MUC16/CA125 is one of the few oldest cancer biomarkers still used in current clinical practice. As mesothelium is an abundant source of MUC16 and a major contributor to stromal heterogeneity in PDAC, we investigated the regulation of MUC16 in tumor and stromal compartments individually. The trajectories constructed using the single-cell transcriptomes of stromal cells from KPC tumors demonstrated continuity in the trajectory path between MUC16-expressing mesothelial cells and other CAF subsets. Further, the tumor tissues of MUC16 whole-body knockout (KPCM) showed dysregulation in the markers of actomyosin assembly and fibroblast differentiation (iCAF and myCAF), indicating that MUC16 has an extra-tumoral role in controlling CAF differentiation. Although we found mesothelium-derivative stromal cells to be bystanders in normal pancreas, the proportion of these cells was higher in invasive PDAC, particularly in TP53 deficient tumors. Moreover, we also detail the regulation of MUC16, KRAS, and SOX9 by TP53 family members (TP53 and TP63) using multi-omics data from knockout models, PDAC cell lines, and human PDAC tissues.
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