Inactivation of Cyclin E1 acts pro-apoptotic and anti-proliferative in primary hepatoma cells and protects from hepatocarcinogenesis in mice
N Moro, R Sonntag, YA Nevzorova, JM Bangen, D Fahrenkamp, D Lambertz, W Hu, N Gassler, G Müller-Newen, R Weiskirchen, M Barbacid, P Sicinski, C Trautwein, C Liedtke · Zeitschrift für Gastroenterologie · 2015 · Heft 01
Bibliografische Angaben
Zusammenfassung
Background & Aims: E-type cyclins (CcnE1, CcnE2) are regulatory subunits of Cyclin-dependent kinase 2 (Cdk2). There is evidence that CcnE/Cdk2 complexes control the transition of quiescent cells into the cell cycle. Surprisingly, genetic deletion of CcnE1, CcnE2 or Cdk2 does not inhibit cell proliferation during embryonic development or liver regeneration. The aim of the present study was to evaluate if E-type cyclins or Cdk2 may have a specific role for hepatocarcinogenesis. Methods: We used genetically modified mice with constitutive deletion of Cyclin E1 (CcnE1-/-) or Cyclin E2 (CcnE2-/-) and conditional knoc…
