Integrative Multi-Omics Reveals TSPAN13 as a Candidate Epithelial–Mesenchymal Transition-Associated Regulator in Prostate Cancer

Abstract

Background: Prostate cancer (PCa) is a malignancy with high metastatic potential and poor prognosis, underscoring the urgent need for effective biomarkers and therapeutic targets to improve clinical management. Methods: An integrative multi-omics analysis combined with machine learning algorithms was performed to identify key diagnostic biomarkers. Candidate genes were validated through extensive functional assays in vitro, including proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) analyses. The tumor-promoting effect of TSPAN13 was further assessed in vivo using xenograft mouse models. Immune cell infiltration patterns were analyzed to explore associations with the tumor microenvironment. Results: An exploratory diagnostic model centered on TSPAN13 was developed. Functional depletion of TSPAN13 significantly suppressed PCa cell proliferation, migration, invasion, and EMT in vitro. These anti-tumor effects were recapitulated in vivo, where TSPAN13 knockdown markedly inhibited tumor growth without significant change in body weight. Furthermore, TSPAN13 expression was correlated with distinct alterations in the immune cell composition within the tumor microenvironment. Conclusions: This study identifies TSPAN13 as a candidate EMT-associated regulator in PCa with potential diagnostic and therapeutic relevance. Our findings provide novel insights into PCa pathogenesis and highlight TSPAN13 as a potential candidate for preclinical exploration, offering potential for strategies targeting epithelial malignancy and modulating the immune microenvironment.