Virus Res. 2020 Apr 16:197973. doi: 10.1016/j.virusres.2020.197973. [Epub ahead of print]
The HBx and HBc of hepatitis B virus can influence Id1 and Id3 by reducing their transcription and stability.
Xia L1, Wang S2, Zhang H3, Yang Y4, Wei J4, Shi Y5, Zou C5, Liu J5, Luo M6, Huang A4, Wang D7.
Author information
1
Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, Chongqing Medical University, Chongqing, China; College of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
2
Department of Dermatology and Cosmetology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China.
3
Department of Clinical Laboratory, Chongqing Health Center for Women and Children, Chongqing, China.
4
Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, Chongqing Medical University, Chongqing, China.
5
College of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
6
Department of Clinical Laboratory, Yubei District People's Hospital, Chongqing, China.
7
Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, Chongqing Medical University, Chongqing, China; College of Laboratory Medicine, Chongqing Medical University, Chongqing, China. Electronic address: [email protected].
Abstract
Hepatitis B virus (HBV) infection is closely related with the occurrence and development of hepatocellular carcinoma (HCC), in which Hepatitis B virus x protein (HBx) and core protein (HBc) play crucial roles. Additionally, inhibitors of differentiation (Id) proteins exhibited significant correlation with liver cancer development. Here, we identified that HBV dramatically inhibited the expression of Id1 and Id3 in both protein and transcriptional levels for the first time, whereas there was little effects of the virus on Id2. Additionally, two HBV coded protein, HBc and HBx, could reduce the expression of Id1 and Id3 distinctly, whereas the other two viral proteins, HBs and HBp were unable to affect theId1 and Id3 proteins. Both the activity inhibitors and activators further confirmed that HBc inhibited the expression of Id1 and Id3 by BMP/Smad signaling pathway. HBx could interact with both Id1 and Id3 at residues 112-136 of HBx protein, and it could inhibit the two Id proteins by accelerating their degradation. This is the first report about HBc and HBx regulating Id1 and Id3, whereas the detailed mechanism associated with above needed further experiments to clarify.