Fig. 4.

MiR-455 and miR-181a repress HK2 expression in EC cells. a The putative binding sites for miR-455, miR-181a and miR-218 in the HK2 3′-UTR. b Pan-cancer analysis of miR-455 expression in various human cancerous tissues, including endometrial (UCEC), relative to their paired normal tissues using BioExpress database. c qRT-PCR analysis of miR-455 expression in EM and EC cells. d Kaplan-Meier overall survival analysis was used to assess EC patients with high or low miR-455 expression based on the TCGA data with KM Plotter. e Western blotting analysis of HK2 expression in HEC-1 cells overexpressing indicated miRNA or Ishikawa cells with indicated miRNA expression knockdown. f Luciferase reporter assays of HEC-1 cells co-transfected with luciferase construct containing the wild-type (WT) HK2 3′-UTR, along with each indicated miRNA mimic or control (Ctr) mimic. g Luciferase reporter assay with Ishikawa cells co-transfected with a luciferase reporter plasmid containing WT or mutant (MUT) HK2 3′-UTR, along with miR-455 inhibitor or Ctr inhibitor. h Cell invasion, sphere formation, glucose consumption, and lactate production of HEC-1 cells transfected with Ctr mimic or miR-455 mimic. HEC-1 cells were transfected with or without miR-455 mimic and treated with TX. Cell survival was examined by a cell viability assay. i Cell invasion, sphere formation, glucose consumption, and lactate production of Ishikawa cells transfected with miR-455 inhibitor or Ctr inhibitor. Ishikawa cells were transfected with or without miR-455 inhibitor and treated with TX. Ishi: Ishikawa *P < 0.05