RHOV Promueve la Progresión del Adenocarcinoma Ductal Pancreático

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy, largely due to late-stage diagnosis, limited therapeutic options, and frequent treatment resistance. Ras homolog family member V (RHOV), a member of the Rho family of small GTPases, has been demonstrated in tumorigenesis in several cancer types. However, its role in PDAC remains undefined. This study aimed to evaluate the clinical significance and functional contribution of RHOV in PDAC progression. The association between RHOV expression and PDAC patient outcomes was assessed using the Human Protein Atlas database and validated in an independent cohort of 114 PDAC specimens by immunohistochemistry. The biological functions of RHOV were interrogated using in vitro cell proliferation, migration, and invasion assays, as well as in vivo xenograft models. Mechanistic investigations focused on RHOV-mediated signaling alterations. High RHOV expression correlated with significantly reduced overall and recurrence-free survival in PDAC patients. RHOV overexpression enhanced PDAC cell proliferation and motility, whereas RHOV knockout suppressed these phenotypes in vitro. Mechanistically, RHOV overexpression activated key components of the MAPK signaling pathway, promoting cell growth, and induced epithelial-mesenchymal transition, facilitating increased migration and invasion. The xenograft studies confirmed that RHOV drives tumor growth and elevates tumor burden in vivo. These findings identify RHOV as a previously unrecognized oncogenic driver in PDAC and suggest its potential utility as a prognostic biomarker and therapeutic target.