Articlenpj aging2025
Endo180 and basement membrane stiffness induce OXPHOS and neoplastic transformation in aging prostate epithelia.
Article in npj aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During prostate aging collagen-IV is modified by advanced glycation end-products, inducing crosslinking of the basement membrane surrounding glandular acini. Basement membrane stiffness sensed by Endo180 disrupts its suppressor complex with CD147, triggering epithelial-to-mesenchymal transition and limiting survival in prostate cancer patients. Here we report basement membrane stiffness and Endo180 cooperate in rewiring epithelia for mitochondrial oxidative phosphorylation (OXPHOS) and growth suppressor evasion, cell proliferation promotion, cell death resistance, inflammation, invasion and metastasis without affecting genome instability, highlighting a non-oncogenic biomechanical event in age-related neoplasia. Endo180-CD147 complex coupled to OXPHOS in Gleason 6 and in Gleason ≥7 tumors Endo180 uncoupled from CD147-OXPHOS, identifying a bio-switch for invasive cancer. Endo180 correlated with patient age in normal tissue, Gleason 6 and 7, but not Gleason 8 tumors, suggesting biological age unleashes its suppression of tumorigenesis. Application of Endo180-based diagnostics in age-related glandular cancers could inform treatment decisions, improving quality of life and survival.
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Registered trials
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