The BH3-only protein BID impairs the p38-mediated stress response and promotes hepatocarcinogenesis during chronic liver injury in mice

摘要: Apoptosis is critical for maintaining tissue homeostasis, and apoptosis evasion considered as a hallmark of cancer. However, increasing evidence also suggests that proapoptotic molecules can contribute to the development cancer, including liver The aim this study was further clarify role B-cell lymphoma 2 homology domain 3 (BH3)-only protein BH3 interacting-domain death agonist (BID) chronic injury (CLI) hepatocarcinogenesis (HCG). Loss BID significantly delayed tumor in two mouse models Fah-mediated HBsTg-driven HCG, suggesting tumor-promoting effect BID. Liver well basal mitogen-stimulated hepatocyte proliferation were not modulated by Moreover, there no vivo or vitro involved DNA damage response hepatocytes hepatoma cells. Our data revealed CLI associated with strong activation oxidative stress (OS) impaired full p38 after OS. Conclusion: We provide function related enhanced an response. In contrast, suppresses activity facilitates malignant transformation hepatocytes. (Hepatology 2015;62:816–828)