ArticleFrontiers in oncology2026
ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- METTL3-Mediated m6A Modification of COL5A2 Inhibits Ferroptosis Through an IGF2BP3-dependent Mechanism in Gastric Cancer.Technology in cancer research & treatmentArticle
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5 authors.
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Abstract
Background: ADAMTS2, a secreted metalloproteinase essential for collagen maturation, exhibits context-dependent roles in cancer but remains uncharacterized in prostate cancer (PCa). Its potential involvement in PCa progression and underlying mechanisms are unknown. Methods: We integrated bioinformatic analysis of TCGA-PRAD data with clinical specimen validation, Results: ADAMTS2 was significantly upregulated in PCa tissues and cell lines, correlating with aggressive clinicopathological features and poor progression-free survival. Functionally, ADAMTS2 promoted PCa cell aggressiveness Conclusions: Our investigation considers ADAMTS2 as a novel oncogenic driver in PCa that promotes tumor progression by reinforcing a tumor-permissive extracellular matrix through upregulation of COL1A1 and by stimulating the FAK/PI3K/AKT pathway to suppress ferroptosis. These findings position ADAMTS2 as a potential predictive biomarker and a valuable therapeutic target for defeating ferroptosis resistance in PCa.
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