Liver specific deletion of CYLDexon7/8 in mice leads to ductular reaction, oval cell activation and increased hepatocellular proliferation after partial hepatectomy

Background: The NF-κB pathway is constitutively activated in various types of cancers and represents a mechanistic link between anti-apoptotic signaling, proliferation and cancer development. NF-κB signaling is negatively controlled by ubiquitin deconjugation mediated by deubiquitinases such as CYLD and A20. The tumor suppressor CYLD is frequently downregulated in hepatocellular carcinoma (HCC), thereby contributing to increased cell cycle progression and proliferation. However, its role for proliferation in the liver is unclear. Aims: In the present study we analyzed the role of CYLD for liver homeostasis and t…