Mitochondrial Slc25a10 Promotes Prostate Cancer Progression By Inhibiting Ferritinophagy Guopeng Yu Kailei Chen Bin Xu Qi Cao by Guopeng Yu & Kailei Chen & Bin Xu & Qi Cao instant download after payment.

Prostate cancer (PCa) is one of the most common malignancies in men worldwide and remains a major cause of cancer-relatedmortality. Despite advances in early diagnosis and treatment, a significant proportion of patients eventually progress to advancedor treatment-resistant disease, highlighting the urgent need for novel therapeutic targets and strategies. In this study, wesystematically analyzed transcriptomic data from The Cancer Genome Atlas (TCGA) and performed Venn analysis to identify genesassociated with PCa progression. Among the intersecting candidates, SLC25A10, a mitochondrial carrier protein, emerged as apotential key regulator of ferroptosis. Further expression analyses revealed that SLC25A10 is significantly upregulated in PCa tissuesand correlates with poor prognosis. Functional gain- and loss-of-function experiments demonstrated that SLC25A10 promotestumor cell proliferation, migration, and invasion, while exacerbating mitochondrial dysfunction and impairing autophagic flux.1234567890();,:Mechanistically, mass spectrometry and co-immunoprecipitation (Co-IP) assays confirmed a direct interaction between SLC25A10and P62, implicating this interaction in the suppression of autophagy and the promotion of ferroptotic vulnerability. Moreover,disruption of the SLC25A10/p62/KEAP1/Nrf2 signaling axis reactivated autophagy and inhibited PCa cell growth. Collectively, ourfindings uncover a novel oncogenic role of SLC25A10 in PCa and suggest that targeting the SLC25A10-mediated regulatorynetwork may offer a promising therapeutic avenue for patients with advanced prostate cancer.Cell Death Discovery (2025) 11:242 ;