Fig. 7: Galectin-3 is implicated in hepatocarcinogenesis.
a CCK-8 assays for the proliferation of HepG2 cells were treated with LPS or LPS and GB1107, or infected with lentiviruses carrying shGFP or shGal3 and transfected with FLAG-metap2 or FLAG-RagAGTP/RagCGDP. Each bar represents the mean ± SD for biological triplicate experiments. P values were calculated by two-way ANOVA (***P < 0.001). b HepG2 cells were treated with LPS, LPS and Torin1, or LPS and GB1107, or infected with lentiviruses carrying shGFP or shGal3 and transfected with FLAG-RagAGTP/RagCGDP in the presence or absence of Torin1 and cultured for 10 days before staining with crystal violet for colony formation assays. Representative images from biological triplicate experiments are shown. c Kaplan–Meier analysis for the correlation between survival time and galectin-3 signatures in HCC. P values were calculated by log-rank test. d Transcriptomes of TCGA primary tumor samples and GTEX normal tissue samples obtained from UCSD Xena for correlation analysis of the expression between galectin-3 and HK2 or PKM. Spearman correlation coefficients and P values were calculated by two-sided permutation test. e Kaplan-Meier analysis for the correlation between survival time and the expression levels of galectin-3 and HK2 or galectin-3 and PKM in HCC. P values were calculated by log-rank test.
