Fig. 6

TCF7L2 and MIR100HG forms a reciprocal positive feedback loop in CRC cells. a Schematic diagram showing the binding motifs of TCF7L2 in the MIR100HG promoter. b Top, Immunoblots of TCF7L2 showing the silencing efficiency of siRNAs against TCF7L2. Bottom, qPCR analysis of MIR100HG expression in CC-CR and HCT116 cells after TCF7L2 knockdown. n = 3 independent biological replicates. c Schematic representation of consecutive deletion or mutation constructs spanning the − 2000 to + 500 region of the MIR100HG promoter. Putative TCF7L2-binding sites in the MIR100HG promoter are indicated in black. d, e Luciferase activity of serially truncated (d) or mutated (e) MIR100HG luciferase reporter constructs transfected into CC-CR and HCT116 cells after TCF7L2 knockdown, n = 3 independent biological replicates. f qPCR assessing the abundance of DNA within the MIR100HG promoter region with a primer pair spanning the TCF7L2-binding sites after ChIP assays with a TCF7L2 antibody or control IgG in CC-CR and HCT116 cells. n = 3 independent biological replicates. g Box plot showing MIR100HG expression in 16 CRC cell lines with low and high TCF7L2 expression. The mean expression of TCF7L2 was used as a cut-off value. h Correlation analysis of TCF7L2 and MIR100HG expression in CRC patients from TCGA dataset (n = 644). (i) Proposed working model in this study. ***P < 0.001, **P < 0.01, *P < 0.05. Data represent mean ± s.d., n.s., not significant