Xue Jing1, Yun-Feng Piao, Ye Liu, Pu-Jun Gao. 1. Department of Hepatology, The First Hospital of Jilin University, Changchun 130021, Jilin Province, People's Republic of China.
Abstract
PURPOSE: This study investigated the effect and clinical significance of beta2-GPI in hepatocellular carcinoma (HCC). METHODS: Double fluorescent immunostaining analysis was performed in paraffin wax-embedded histological sections of nine HCC parenchyma, seven adjacent non-cancerous tissues and seven control liver tissues from hepatitis B virus (HBV) infected patients using a beta2-GPI polyclonal antibody and a HBV surface antibody. NF-κB activation was assessed by a non-radioactive electrophoretic mobility shift assay (EMSA) and immunofluorescence assay in SMMC-7721 HCC cells exposed to various treatments. The cells were transiently transfected with vectors expressing beta2-GPI (group one), HBsAg (group two), both beta2-GPI and HBsAg (group three), or with a control vector (group four). Untransfected cells (group five) were also used as a control. Alpha fetoprotein (AFP) expressions were also detected by ELISA in all groups. RESULTS: The highest degree of co-localization of beta2-GPI and HBsAg proteins was seen in the endochylema and occurred at the nuclear border in the cancer tissues. Weak beta2-GPI protein staining was present in the endochylema, with a strong signal for HBsAg protein in HBV control samples. Adjacent non-tumorous liver tissue samples also showed HBsAg staining but stronger beta2-GPI signals in the endochylema. In experiments with SMMC-7721 HCC cells, groups one and two had induced activation of NF-κB with the relative NF-κB DNA-binding activities of 55.84 and 51.12, respectively. However, the highest relative NF-κB DNA-binding activity was observed in group three (80.5). The percentages of cells with NF-κB translocated from the cytoplasm to nucleus in groups one, two, three, four and five compared with total cells were 13.5, 8.7, 24.9, 5.7 and 0.95%, respectively. The mean AFP levels were significantly higher in group three (0.0640 ± 0.0059) than in group five (P < 0.001). It appeared higher in group three than in group one (0.0562 ± 0.0060, P < 0.05) and group four (0.0585 ± 0.0040, P < 0.05), while no significant differences were seen between groups three and two, and between groups four and five. CONCLUSIONS: Beta2-GPI may play a role in the development of HBV-related HCC by activating NF-κB via interaction of beta2-GPI and HBsAg.
PURPOSE: This study investigated the effect and clinical significance of beta2-GPI in hepatocellular carcinoma (HCC). METHODS: Double fluorescent immunostaining analysis was performed in paraffin wax-embedded histological sections of nine HCC parenchyma, seven adjacent non-cancerous tissues and seven control liver tissues from hepatitis B virus (HBV) infectedpatients using a beta2-GPI polyclonal antibody and a HBV surface antibody. NF-κB activation was assessed by a non-radioactive electrophoretic mobility shift assay (EMSA) and immunofluorescence assay in SMMC-7721 HCC cells exposed to various treatments. The cells were transiently transfected with vectors expressing beta2-GPI (group one), HBsAg (group two), both beta2-GPI and HBsAg (group three), or with a control vector (group four). Untransfected cells (group five) were also used as a control. Alpha fetoprotein (AFP) expressions were also detected by ELISA in all groups. RESULTS: The highest degree of co-localization of beta2-GPI and HBsAg proteins was seen in the endochylema and occurred at the nuclear border in the cancer tissues. Weak beta2-GPI protein staining was present in the endochylema, with a strong signal for HBsAg protein in HBV control samples. Adjacent non-tumorous liver tissue samples also showed HBsAg staining but stronger beta2-GPI signals in the endochylema. In experiments with SMMC-7721 HCC cells, groups one and two had induced activation of NF-κB with the relative NF-κB DNA-binding activities of 55.84 and 51.12, respectively. However, the highest relative NF-κB DNA-binding activity was observed in group three (80.5). The percentages of cells with NF-κB translocated from the cytoplasm to nucleus in groups one, two, three, four and five compared with total cells were 13.5, 8.7, 24.9, 5.7 and 0.95%, respectively. The mean AFP levels were significantly higher in group three (0.0640 ± 0.0059) than in group five (P < 0.001). It appeared higher in group three than in group one (0.0562 ± 0.0060, P < 0.05) and group four (0.0585 ± 0.0040, P < 0.05), while no significant differences were seen between groups three and two, and between groups four and five. CONCLUSIONS:Beta2-GPI may play a role in the development of HBV-related HCC by activating NF-κB via interaction of beta2-GPI and HBsAg.
Authors: I Stefas; M Rucheton; A D D'Angeac; C Morel-Baccard; J M Seigneurin; J P Zarski; M Martin; M Cerutti; J P Bossy; D Missé; H Graafland; F Veas Journal: Hepatology Date: 2001-01 Impact factor: 17.425
Authors: Stanislav Naryzhny; Natalia Ronzhina; Elena Zorina; Fedor Kabachenko; Nikolay Klopov; Victor Zgoda Journal: Int J Mol Sci Date: 2022-09-21 Impact factor: 6.208