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Background and purpose: XB130 protein plays an important role in proliferation and invasiveness of tumor cells. However, there is little research on the role of XB130 protein in hepatocellular carcinoma (HCC) and the effect of XB130 is still unclear. This study investigated the role of XB130 gene in the proliferation of HCC cell and its potential mechanism. Methods: The protein expressions of XB130 in HCC cell lines, Huh7, HepG2 and SNU449, and liver cell line HL7702 were detected by Western blot. Huh7 cells were transfected with XB130-siRNA. Then cell viability was measured using cell counting kit-8 (CCK-8), and cell cycle was examined by flow cytometry. Protein expressions of p-AKT, p-GSK3β, cyclin D1 and p-Rb were detected by Western blot, while mRNA expression levels of E2F/DP1 target genes (cyclin E1, c-Myc and PCNA) were measured by reverse transcription-polymerase chain reaction (RT-PCR). Results: The relative protein expressions of XB130 in Huh7, HepG2, SNU449 and HL7702 cells were 0.66±0.10, 0.78±0.11, 0.83±0.08 and 0.32±0.06, respectively. The difference between HCC cell lines and HL7702 cell line was statistically significant (P＜0.01). The transfection efficacy of XB130-siRNA was confirmed to be highly effective in Huh7 cells, and the viability of XB130-siRNA transfected Huh7 cells declined 72 h after transfection (P＜0.001). The ratio of Huh7 cells in G0/G1 phase was increased, while the ratio in S or G2/M was decreased 48 h after XB130-siRNA transfection (P＜0.01). In addition, compared with negative control, protein expressions of p-AKT, p-GSK3β, cyclin D1 and p-Rb, and mRNA expression levels of cyclin E1, c-Myc and PCNA were all decreased in XB130-siRNA transfected Huh7 cells (P＜0.001). Conclusion: XB130 promotes the proliferation of HCC cells by regulating cell cycle-related proteins and downstream transcription factors.
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Objective To determine the expression of CD38 and HLA -DR on CD +8 T cells in patients with chronic hepatitis B and HBV carriers,and to disscuss the relation between immune activation and disease progression of HBV infection.Methods Thirty -two chronic hepatitis B patients receiving adefovir dipivoxil treatment,31 HBV carriers and 28 normal controls were collected.The counts of CD +4 and CD +8 T cells and the percentage of CD +8 CD +38 and CD +8 HLA -DR +T cells were tested by flow cytometry.HBV DNA and liver function were tested in the central laboratory of our hospital.Results The percentage of CD +8 CD +38 T cells in CHB patients was (58.4 ±12.7)%,and was higher than that in HBV carriers (46.8 ±8.5)% and normal controls (46.8 ±8.5)%,and decreased after adefovir dipivoxil treatment (34.2 ±9.4%)(F =8.27,P =0.000).The percentage of CD +8 CD +38 T cells in HBV carriers was (43.3 ±12.5)%,and was much higher than that in normal controls (9.8 ±5.7)%(F =13.48,P =0.000).The percentage of CD +8 HLA -DR + T cells in CHB patients was higher than that in normal controls,but similar to that in HBV carriers (37.1 ±11.3)%.CD +8 HLA -DR + T cells in CHB patients also decreased after adefovir dipivoxil treatment (P <0.05 ).Conclusion Our study demonstrates that activation of CD +8 T cells is increased in HBV infection but decreased by adefovir dipivoxil treatment.The percentages of CD +8 CD +38 and CD8 +HLA -DR +T are good markers for disease progression of HBV infection.