Abnormal expression of GP73 in peripheral blood CD4+ T lymphocytes of patients with hepatocellular carcinoma and its related mechanism
10.3969/j.issn.1671-8348.2017.33.021
- VernacularTitle:GP73在肝癌患者外周血CD4+T淋巴细胞中的异常表达及其相关机制研究
- Author:
Shuqun LI
1
;
Jun WENG
;
Qingrong MO
;
Yaqun YU
Author Information
1. 桂林医学院附属医院肝胆胰外科
- Keywords:
liver neoplasms;
GP73;
tumor immunology;
CD4+ T lymphocytes
- From:
Chongqing Medicine
2017;46(33):4667-4669,4672
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the abnormal expression of Golgi protein 73(GP73) in CD4+ T lymphocytes of the pa-tients with hepatocellular carcinoma (HCC) and its influence of Th1/Th2/Th17 subtype differentiation .Methods Fifty cases of HCC hospitalized in this hospital from May 2015 to February 2016 and 50 healthy volunteers as controls were selected .Peripheral blood was collected and CD4+ T lymphocytes were isolated ;then the expression levels of GP73 and nuclear factor kappa-light-chain-enhancer (NF-κB) in CD4+ T lymphocytes were determined by using RT-qPCR and Western blotting methods ;furthermore ,the se-cretion levels of IL-4 ,IL-17 and IFN-γin the supernatants were examined by using ELISA method .Results GP73 mRNA expres-sion in peripheral blood CD4+ T lymphocytes in the HCC patients were significantly up-regulated compared with the healthy volun-teers ,the difference was statistical difference (P<0 .05) .The expression level of in GP73 overexpression group was significantly in-creased(P<0 .05) ,while which in the GP73 interference group was significantly decreased (P<0 .05) .Over-expression of GP73 in-duced significant increase of IL-4 and IL-17 levels and significant decrease of IFN-γ(P<0 .05);silencing GP73 induced marked de-crease in the expression of IL-4 and IL-17 in CD4+ cells and obvious increase of IFN-γ(P<0 .05) .Conclusion GP73 is over-ex-pressed in peripheral blood CD4+ T cells of HCC patients ,moreover GP73 is very likely to participate in the inflammatory reaction by activating NF-κB to cause the unbalance of Th1/Th2/T17 and promote the occurrence and development of HCC .
