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Ding et al. Hepatoma Research 2018;4:12 Hepatoma Research
DOI: 10.20517/2394-5079.2018.07
Case Report Open Access
Beta2-glycoprotein I cooperate with hepatitis
B surface antigen promotes hepatocellular
carcinogenesis via the nuclear factor kappa B signal
pathway were enhanced by the lipopolysaccharide
2
1
1
1
Xue-Li Ding *, Xue Jing *, Nai-Jun Han , Zi-Bin Tian , Pu-Jun Gao , Lin Yang , Ya-Nan Yu 1
1
3
1 Department of Gastroenterology, the Affiliated Hospital of Qingdao University, Qingdao 266003, Shandong, China.
2 Department of Research and development, Yebio Bioengineering Co., Ltd. of Qingdao, Qingdao 266114, Shandong, China.
3 Department of Hepatology, the First Hospital of Jilin University, Changchun 310021, Jilin, China.
*Authors contributed equally
Correspondence to: Dr. Xue Jing, Department of Gastroenterology, the Affiliated Hospital of Qingdao University, No.16 Jiangsu Road,
Qingdao 266003, Shandong, China. E-mail: qdu-jingxue@foxmail.com
How to cite this article: Ding XL, Jing X, Han NJ, Tian ZB, Gao PH, Yang L, Yu YN. Beta2-glycoprotein I cooperate with hepatitis B surface
antigen promotes hepatocellular carcinogenesis via the nuclear factor kappa B signal pathway were enhanced by the lipopolysaccharide.
Hepatoma Res 2018;4:12. http://dx.doi.org/10.20517/2394-5079.2018.07
Received: 11 Feb 2018 First Decision: 8 Mar 2018 Revised: 30 Mar 2018 Accepted: 2 Apr 2018 Published: 28 Apr 2018
Science Editor: Guang-Wen Cao Copy Editor: Guang-Zhe Zhu Production Editor: Huan-Liang Wu
Abstract
Aim: We aimed to elucidate whether beta2-glycoprotein I (β2GPI) cooperation with hepatitis B surface antigen
(HBsAg) promoted hepatocellular carcinogenesis enhanced by the lipopolysaccharide (LPS) via activation of
nuclear factor kappa B (NF-κB) and expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and
alpha fetal protein (AFP) in liver cancer cells.
Methods: Liver cancer cells (SMMC-7721) were transiently transfected with β2GPI and/or HBsAg and were
subjected to LPS treatment. TNF-α, IL-1β, and AFP expression were measured in all groups by ELISA. NF-κB
activation was assessed by non-radioactive electrophoretic mobility shift assay (EMSA) and was quantified in all
groups.
Results: Cells transfected with β2GPI and/or HBsAg induced activation of NF-κB, with the highest activation
seen in the doubly β2GPI- and HBsAg-transfected cells treated with LPS. Non-transfected cells treated with LPS
exhibited lower activation compared to either β2GPI- or HBsAg-transfected cells with LPS treatment. In addition,
cells transfected with β2GPI and/or HBsAg induced significantly increased expression of TNF-α, IL-1β and AFP,
with the highest levels again seen in the doubly β2GPI- and HBsAg-transfected cells treated with LPS.
Conclusion: These observations suggest that the activity of NF-κB induced by β2GPI and HBsAg was enhanced by
LPS. Expression of TNF-α, IL-1β and AFP increased in β2GPI and HBsAg cotransfected liver cancer cells.
© The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
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