Fig. 7
From: Long non-coding RNA ROR decoys gene-specific histone methylation to promote tumorigenesis
ROR repels endogenous G9A methyltransferase. a ChIP assay demonstrating that ROR blocked the recruitment of G9A to the TESC promoter. IgG is used as a native control. T1 through T4 and T11 through T12: primer names; arrow: transcriptional direction; sites X, Y and W: ChIP detecting sites; grey box: exons of TESC genes. b, c The qPCR-ChIP assay showing the interaction of G9A with the TESC promoter. The detection of ChIP sites on the chromosome is listed at the bottom. IgG: native control. All of the data are presented as the mean ± SD. *P <0.05: compared with the control and mock. d Decoy model of ROR regulation in tumorigenesis. In normal cells, ROR lncRNA was silenced and the G9A methyltransferase could freely modify the TESC promoter and provide histone H3K9 methylation to depress TESC expression; however, in cancer cells, ROR was abnormally activated and blocked the G9A interaction with the TESC promoter, and free G9A failed to methylate the TESC promoter and induced aberrant TESC expression, triggering tumorigenesis