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. 2022 Mar 30;298(5):101885. doi: 10.1016/j.jbc.2022.101885

Figure 6.

Figure 6

EPO is inversely correlated to hCAR expression in HCC and promotes proliferation of HepG2 and Hep3B cells.A, hCAR and EPO gene expression was inversely correlated in patients with HCC. A total of 381 HCC samples were analyzed from a publicly accessible TCGA database through SurvExpress, and the overall survival was compared between low-hCAR–expressing (123), medium-hCAR–expressing (232), and high-hCAR expressing (26) groups. B, correlation analysis between hCAR and EPO reveal a Spearman’s correlation coefficient of −0.20 (p < 0.01). C, the pair of low hCAR with high EPO is associated with poor survival. D, in HepG2-hCAR and Hep3B-hCAR cells, treatment with Dox resulted in increased expression of hCAR and decreased expression of EPO in a concentration-dependent manner. E, expression of EPO in HepG2 cells was efficiently abolished after EPO knockdown via lentivirus shRNA targeting different regions of EPO (shEPO 1 to shEPO 5). F, depletion of EPO in HepG2 and Hep3B cells results in suppression of cell growth in a time-dependent manner. HepG2 and Hep3B cells were also visualized by Coomassie blue staining 8 days after infection with lentivirus shEPO 1, shEPO 3, or shCon. G, relative cell growth rate of HepG2-hCAR cells treated with Dox was partially rescued by addition of the recombinant human EPO treatment. Results are expressed as mean ± SD from three independent experiments in D–G. ##p < 0.01; ∗p < 0.05; and ∗∗p < 0.01. Dox, doxycycline; EPO, erythropoietin; hCAR, human constitutive androstane receptor; HCC, hepatocellular carcinoma; TCGA, The Cancer Genome Atlas.