ArticleMolecular cancer2025
c-Rel drives pancreatic cancer metastasis through fibronectin-integrin signaling-induced isolation stress resistance and EMT.
Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Spatial co-expression and cell-cell communication inference from spatially resolved transcriptomics with CONCISE.bioRxiv : the preprint server for biology · 2026Article
- Stress-responsive membrane proteins as execution nodes of tumor cell adaptation to microenvironmental stress.Oncogene · 2026Review
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Abstract
backgroundPancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest malignancies, with limited treatment options and a high recurrence rate. Recurrence often occurs with metastasis, for which cancer cells must adapt to isolation stress to successfully colonize distant organs. While the fibronectin–integrin axis has been implicated in this adaptation, its regulatory mechanisms require further elaboration.
methodsWe utilized genetically engineered PDAC mouse models with c-Rel knockout, overexpression and fibronectin (FN1) depletion, alongside in vitro assays, to assess EMP, extracellular matrix (ECM) remodeling, and resistance to anchorage-independent growth. Functional analyses, including transcriptomics, Cut&Run, flow cytometry, immunohistochemistry, and metastatic assays, were performed to elucidate the role of c-Rel in fibronectin–integrin signaling during PDAC progression.
resultsWe identified c-Rel as an oncogenic driver in PDAC that promotes EMP, ECM remodeling, and survival under isolation stress. c-Rel directly regulates FN1 and CD61/integrin β3 (ITGB3) transcription, enhancing cellular adaptability in metastatic settings. While FN1 is dispensable for EMT, its absence significantly impairs metastatic colonization and anchorage-independent growth.
conclusionsOur findings suggest that c-Rel can regulate PDAC progression and metastasis by modulating the tumor microenvironment and stress resistance. Targeting the c-Rel–fibronectin–integrin axis may offer novel therapeutic strategies to mitigate disease progression.
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