HBsAg/ β2GPI activates the NF‑κB pathway via the TLR4/MyD88/IκBα axis in hepatocellular carcinoma.

HBsAg/β2GPI activates the NF‑κB pathway via the TLR4/MyD88/IκBα axis in hepatocellular carcinoma. Oncol Rep. 2018 Jun 19;: Authors: Jing X, Tian Z, Gao P, Xiao H, Qi X, Yu Y, Ding X, Yang L, Zong L Abstract Chronic hepatitis B virus (HBV) infection remains one of the leading causes of hepatocellular carcinoma (HCC) globally. However, the mechanism underlying the mediation by HBV surface proteins (HBsAgs) of the early steps in the virus life cycle and following HCC development is unclear. β‑2‑glycoprotein I (β2GPI) specifically interacts with HBsAg and demonstrates high expression during the earliest stages of hepatitis B virus infection. In the present study, the assessment of HCC and adjacent tissues revealed that the levels of mRNA and protein of β2GPI were highly expressed in HBV‑related HCC. Previous studies have reported that HBsAg activates the nuclear factor (NF)‑κB pathway via interaction with β2GPI in HCC. However, the underlying mechanism of how the interaction between HBsAg and β2GPI confers activation of the NF‑κB pathway is still unclear. The HBsAg is comprised of three carboxyl‑co‑terminal HB proteins. In the present study, immunofluorescence assay and EMSA consistently revealed that a combination of recombinant small HBV surface antigen (rSHB) and β2GPI can significantly activate the NF‑κB signaling pathway. Another study from our team revealed that high expression of β2GPI enhanced H...
Source: Oncology Reports - Category: Cancer & Oncology Tags: Oncol Rep Source Type: research