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. 2021 Jun 23;9:664375. doi: 10.3389/fcell.2021.664375

FIGURE 3.

FIGURE 3

JHDM1D/KDM7A mediates TGF-β-induced RHOJ transcription. (A–H) MCF7 (left panel) and T47D cells (left panel) were transfected with indicated siRNAs followed by treatment with TGF-β for 48 h. Knockdown efficiencies were validated by Western blotting (A). RHOJ expression was examined by qPCR (B) and Western blotting (C). ChIP assays were performed with anti-H3K9Me2 (D), anti-H3K27Me2 (E), anti-RNA polymerase II (F), anti-TBP (G), and anti-TFIID (H). All experiments were performed in triplicate wells and repeated three times, and one representative experiment is shown. Data represent mean ± SD. *p < 0.05, two-tailed t-test. KDM7A mediated RHOJ trans-activation by removing H3K9/H3K27 methylation to facilitate the recruitment of RNA polymerase II, TBP, and TFIID to the RHOJ promoter. (I) Expression data were extracted from the public database to draw the scatter plot. Pearson correlation coefficient was calculated. Positive correlation between KDM7A expression and RHOJ expression was identified in human breast cancer tissues.