Fig. 6

Functional roles of IL-6-RAD51B-UBE2D1 axis in HCC. a Cell numbers in continuous IL-6 treated QSG-7701 were determined by CCK-8 assay, and the relative number of cells is shown in mean ± standard error. b Plate clone formation assays for QSG-7701 cells treated with continuous IL-6. The number of colonies was showed in the right panel. c and d Cell proliferation by CCK-8 assays (c) and clone formation assays (d) to evaluate the roles of STAT3 and RAD51B under continuous IL-6 pressure. e and f Apoptosis in indicated QSG-7701 cells by Western blotting of apoptosis markers (e) or TUNEL assays (f). IL-6-LT/UBE2D1 gain indicated cell clones with UBE2D1 gains after 4 months IL-6 stimulation. IL-6-LT here indicated cell clones without UBE2D1 gains after 4 months IL-6 stimulation. The value of TUNEL score was showed in the right panel. g The relative expression of RAD51B in HCC patients with high serum IL-6 and low serum IL-6. y, the relative expression of RAD51B in HCC compared with nontumor tissues. x, the median intensity was used as the cutoff for low and high group. Independent-Sample T test was adopted for the statistical analysis. h The transcript level of RAD51B were determined by real-time PCR in HCC and paired adjacent nontumor tissues in HCC Cohort (n = 108). β-actin was used as internal control. i Relative expression of RAD51B in precancerous lesions and paired nontumor tissues without lesions(n = 9). Wilcoxon signed-rank test was adopted for the statistical analysis. j Kaplan-Meier analyses of the correlations between relative intensity of RAD51B in nontumor tissues in GSE14520 and recurrence-free survival of HCC patients. The median intensity was used as the cutoff for low and high group. *p < 0.05,**p < 0.01, ***p < 0.001