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

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Copyright © 2021 Zhang, Chen, Zhu, Zhang, Zhang, Yuan and Xu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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H3K9 dimethylation and H3K27 dimethylation explain differential RHOJ expression. (A–D) MCF7 (left panel) and T47D (left panel) cells were transfected with indicated siRNAs followed by treatment with TGF-β for 48 h. ChIP assays were performed with anti-H3Ac (A), anti-H3K4Me3 (B), anti-H3K9Me2 (C), and anti-H3K27Me2 (D). 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. MKL1 depletion partially restored H3K9/H3K27 dimethylation without altering H3 acetylation or H3K4 trimethylation on the RHOJ promoter.