Interleukin-17A facilitates tumor progression via upregulating programmed death ligand-1 expression in hepatocellular carcinoma

Figure 3 Interleukin-17A upregulated programmed cell death ligand-1 expression via the interleukin-17A receptor/p-small mothers against decapentaplegic 2 signaling pathway in hepatocellular carcinoma cells. A: The Cancer Genome Atlas results revealed that interleukin-17A (IL-17A) and small mothers against decapentaplegic 2 (SMAD2) expression was increased in hepatocellular carcinoma (HCC) samples compared with normal tissue samples; B: Interleukin-17A receptor (IL-17RA) protein expression level after knockout (KO) of IL-17RA in Huh7 cells; C: IL-17RA mRNA levels after KO of IL-17RA in Huh7 cells; D: IL-17RA KO alone did not affect programmed cell death ligand-1 (PD-L1) expression in Huh7 cells; E: IL-17A-induced PD-L1 expression was reversed by IL-17RA KO in Huh7 cells; F: IL-17A increased the level of phosphorylated (p)-SMAD2 in HCC cells; G: IL-17A-induced PD-L1 expression was inhibited by pretreatment with transforming growth factor-beta signal pathway inhibitor in HCC cells; H: IL-17RA KO sharply reversed IL-17A-induced p-SMAD2 expression in Huh7 cells. ^aP < 0.05; ^bP < 0.01; ^cP < 0.001; ^dP < 0.0001. ITD: TGF-beta signal pathway inhibitor; MOCK: Blank control; NC: Negative control.