ArticleJournal of experimental & clinical cancer research : CR2025
Reciprocal regulation of MMP-28 and EGFR is required for sustaining proliferative signaling in PDAC.
Article in Journal of experimental & clinical cancer research : CR, 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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Who cites it
2 citing papers in PubMed.
- Pancreatic ductal adenocarcinoma: integrating molecular insights for targeted interventions.Signal transduction and targeted therapy · 2026Review
- Innate immune cell barrier-related genes inform precision prognosis in pancreatic cancer.Frontiers in immunology · 2025Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroudSustaining proliferation signaling is the top hallmarks of cancer, driving continuous tumor growth and resistance to drug treatments. Blocking proliferation signaling has shown limited benefit in clinical treatment of pancreatic ductal adenocarcinoma, highlighting the urgent need to deeply understand proliferation signaling and develop new therapeutic strategies.
methodsBy leveraging clinical data and data from the TCGA and GDSC datasets, we investigated the association between MMP-28 expression and the sensitivity to EGFR inhibitors as well as the prognosis of PDAC. Transcriptomic and biological experiments explore the regulatory role of MMP-28 on the EGFR signaling pathway. Additionally, in vitro and in vivo studies are employed to evaluate MMP-28 as a biomarker for sensitivity to EGFR inhibitors.
resultsWe found that MMP-28, a metalloproteinase, was significantly associated with the sensitivity to EGFR inhibitors. Furthermore, MMP-28 could promote PDAC growth and metastasis. Mechanistically, MMP-28 facilitated the maturation and release of the TGF-α precursor, thus promoting EGFR activation. In return, EGFR upregulated MMP-28 through AP-1-mediated transcription, forming a positive feedback loop that provided sustaining proliferation signaling for PDAC. Subsequently, MMP-28 was identified to predict the response to EGFR inhibitors and recognize responsive patients.
conclusionsOur findings revealed the role of MMP-28 and EGFR in generation of sustaining proliferation signaling and provided a new therapy strategy for PDAC.
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