Pharmacological inhibition of FAK reversed both the oncogenic and anti-ferroptotic effects of ADAMTS2.<h4>Conclusions</h4>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. Here, COL1A1 is linked to neoplasm.