Inhibition of canonical IKK/NF-kB signaling in Hepatitis B Virus surface antigen transgenic mice drastically increases HCC development due to dysregulated Unfolded Protein Respons…
Y Sunami, M Ringelhan, M Lu, N Hüser, E Kokai, F Leithäuser, J Kleeff, S Gul, S Wissel, D Hartmann, RM Schmid, H Friess, C Brunner, P Riedl, R Schirmbeck, P Strnad, M Heikenwälder, T Wirth · Zeitschrift für Gastroenterologie · 2015 · Heft 01
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Zusammenfassung
Background and Aims: Hepatitis B Virus (HBV) remains the most common risk factor for hepatocellular carcinoma (HCC). It has been suggested that, in addition to chronic inflammation, HBV viral products directly contribute in HBV-driven hepatocellular carcinogenesis. In patients with low HBV replication, it is proposed that accumulation of HBV surface antigen (HBsAg) in the endoplasmic reticulum (ER) of hepatocytes (referred to as “ground glass hepatocytes”) activates ER stress, directly driving carcinogenesis. In the ER stress response, NF-kB is known to be important for the control of the Unfolded Protein Respon…
