Ras Homolog Family Member V Promotes Pancreatic Ductal Adenocarcinoma Progression.

Area of Science:

• Oncology
• Molecular Biology
• Cancer Research

Background:

• Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer with limited treatment options.
• The role of Ras homolog family member V (RHOV) in PDAC pathogenesis is currently unknown.

Purpose of the Study:

• To investigate the clinical significance of RHOV expression in PDAC.
• To elucidate the functional role and underlying mechanisms of RHOV in PDAC progression.

Main Methods:

• RHOV expression analysis in PDAC patient cohorts (Human Protein Atlas, immunohistochemistry).
• In vitro assays (proliferation, migration, invasion) and in vivo xenograft models to assess RHOV function.
• Mechanistic studies on RHOV-mediated signaling pathways (MAPK, epithelial-mesenchymal transition).

Main Results:

• High RHOV expression is significantly associated with poorer overall and recurrence-free survival in PDAC patients.
• RHOV overexpression promotes PDAC cell proliferation, migration, and invasion in vitro.
• RHOV activates MAPK signaling and epithelial-mesenchymal transition, driving tumor growth and burden in vivo.

Conclusions:

• RHOV acts as an oncogenic driver in pancreatic ductal adenocarcinoma.
• RHOV represents a potential prognostic biomarker and therapeutic target for PDAC.