Fig. 6
From: BOK promotes chemical-induced hepatocarcinogenesis in mice
Schematic model of how BOK contributes to DEN-induced HCC. BOK levels in the liver are increased in the short-term response to DEN and BOK contributes to liver damage upstream of BIM and PUMA induction. As a consequence of reduced cell death, associated inflammation and compensatory proliferation, Bok-/- mice develop fewer HCC tumors in the long term. Additionally, BOK has a likely cell death-independent function of positively modulating cellular proliferation of HCC cells, resulting in smaller tumors in Bok-/- mice
