Fig. 4

TP73-AS1 competed with HMGB1 for miR-200a binding a miR-200a inhibitor was transfected into HCCLM3 and HepG2 cells to achieve miR-200a inhibition. The inhibitory efficiency was verified by using real-time PCR. b TP73-AS1 expression in response to ectopic miR-200a expression and inhibition in HCCLM3 and HepG2 cells was determined by using real-time PCR. c miR-200a expression in response to TP73-AS1 knockdown in HCCLM3 and HepG2 cells was determined by using real-time PCR. d A wt-TP73-AS1 luciferase reporter vector (wt-TP73-AS1), as well as a mut-TP73-AS1 luciferase reporter vector (mut-TP73-AS1) by sequentially mutating the predicted two miR-200a binding sites in TP73-AS1 was constructed. A wt-HMGB1 3’UTR luciferase reporter vector (wt-HMGB1 3’UTR), as well as a mut-HMGB1 3’UTR luciferase reporter vector (mut-HMGB1 3’UTR) by sequentially mutating the predicted miR-200a binding sites in the 3’UTR of HMGB1 was constructed. e The wt-HMGB1 3’UTR/mut-HMGB1 3’UTR vectors and miR-200a inhibitor/miR-200a mimics were co-transfected into HepG2 cells. The luciferase activity of the wt- or mut-HMGB1 3’UTR luciferase reporter vector was determined by using dual luciferase assays. f The wt-TP73-AS1/mut-TP73-AS1 vectors and miR-200a inhibitor/miR-200a mimics were co-transfected into HepG2 cells. The luciferase activity of the wt- or mut-TP73-AS1 luciferase reporter vector was determined by using dual luciferase assays. The data are presented as mean ± SD of three independent experiments. *P < 0.05, **P < 0.01