Page 175 - Read Online
P. 175

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
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


                                                                                                                                                    www.hrjournal.net
   170   171   172   173   174   175   176   177   178   179   180