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. 2014 Sep 3;5(20):9783–9797. doi: 10.18632/oncotarget.2392

Figure 5. Mechanisms of progressive PR silencing in endometrial cancer cells.

Figure 5

(A) ChIP followed by q-PCR analysis of SUZ12, H3K9Ace or H3K9Me3 recruitment to the PGR promoter. (B) ChIP-PCR analysis. Ishikawa H cells were treated with or without 20 nM LBH589 for 24h, and Hec50 cells were treated with or without the hypomethylating agent 100 nM 5-aza-deoxycytidine (5-aza) for 5 days. ChIP followed by q-PCR for SUZ12 and H3K9Ace was used to determine recruitment of these factors to the PGR promoter. (C) ChIP-PCR analysis. ChIP followed by q-PCR for RNA polymerase II (RNA PII) and H3K9 trimethylation (H3K9Me3) was performed to assess occupancy on the PGR promoter. (D) Proposed model for PR repression in well-differentiated and poorly-differentiated endometrial cancer. In well-differentiated endometrial cancers, PR was transcriptional repressed by PRC2 and reversed by HDACi treatment, while in poorly-differentiated endometrial cancers, PR was suppressed by DNA methylation and reversed by a hypomethylating agent.