Journal
VIRUS RESEARCH
Volume 293, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.virusres.2020.198264
Keywords
HBV; C-terminal truncation; HBx; FXR; HCC
Categories
Funding
- National Natural Science Foundation of China [81772972, 81572703]
- Guangdong Natural Science Foundation [2015A030313449]
- Guangdong Provincial Science and Technology Program [2014A020212285]
- Department of Education, Guangdong Government under the Top-tier University Development Scheme for Research and Control of Infectious Diseases [2016026, 2015060, 2015089]
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The study found that both full-length HBx and HBx C-terminal truncation coexist in HCC, and both can activate FXR signaling. Additionally, HBx-C30 has a weaker coactivating effect on FXR-KNG1 signaling compared to full-length HBx.
Hepatitis B virus (HBV) X protein (HBx) is a key regulator of HBV-associated hepatocarcinogenesis. C-terminal-truncated HBx is frequently detected in hepatocellular carcinoma (HCC). The role of HBx, especially C-terminal-truncated HBx, in HCC pathogenesis has been controversial. To elucidate the biological role of C-terminal-truncated HBx underlying HBV-associated hepato-oncogenesis, we constructed a vector expressing HBx-C30 (deletion of 30 as from the C terminus of HBx) and functionally analyzed its regulation on farnesoid X receptor (FXR) signaling, which is known to inhibit hepatocarcinogenesis. In the present study, we found full-length HBx and HBx C-terminal truncation coexist in HCC, and both full length HBx and HBx-C30 can activate FXR signaling. Moreover, HBx-C30 weakly coactivates FXR-KNG1 signaling compared to full-length HBx.
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