Progression of liver oncogenesis in the double transgenic mice c-myc/TGF α is not enhanced by cyclooxygenase-2 expression.

LLORENTE-IZQUIERDO C; MAYORAL R; CUCARELLA C; GRAU C; ALVAREZ MS; FLORES JM; GARCÍA-PALENCIA P; AGRA N; CASTRO-SÁNCHEZ L; BOSCÁ L; MARTÍN-SANZ P; CASADO M

PROSTAGLANDINS & OTHER LIPID MEDIATORS

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2013

1098-8823

Cyclooxygenase-2 (COX-2) has been associated with cell growth regulation, tissue remodeling and carcinogenesis. Overexpression of COX-2 in hepatocytes constitutesan ideal condition to evaluate the role of prostaglandins (PGs) in liverpathogenesis. The effect of COX-2-dependent PGs in genetic hepatocarcinogenesishas been investigated in triple c-myc/transforming growth factor α (TGF-α)transgenic mice that express human COX-2 in hepatocytes on a B6CBAxCD1xB6DBA2background. Analysis of the contribution of COX-2-dependent PGs to thedevelopment of hepatocarcinogenesis, evaluated in this model, suggested a minorrole of COX-2-dependent prostaglandins to liver oncogenesis as indicated by liverhistopathology, morphometric analysis and specific markers of tumor progression. This allows concluding that COX-2 is insufficient for modifying thehepatocarcinogenesis course mediated by c-myc/TGF-α.