The Effects Of Histone Demethylase JARID1A On Proliferation And Its Mechanism In Human Endometrial Cancer Ishikawa Cells

ObjectiveTo investigate the effects of histone demethylase JARID1A on proliferationin human endometrial cancer cells in vitro, and its possible mechanism, inorder to provide a new target for endometrial cancer gene therapy.Method1. The effects of histone demethylase JARID1A on proliferation in humanendometrial cancer Ishikawa cells. The JARID1A siRNA were transfectedinto Ishikawa cells; MTT and Flow cytometry were used to evaluate thecells proliferation and cycle.2. The mechanism of inhibition of histone demethylase JARID1A onproliferation in endometrial cancer Ishikawa cells. The expression of PRwas detected by RT-qPCR and Western-blot, which was interfered with theJARID1A siRNA; The pCMV-HA-JARID1A and pCMV-HA recombinantplasmids were respectively transfected into Ishikawa cells withLipofectamineTM2000reagent, The PR expression was detected byRT-qPCR and Western-blot; The H3K4trimethylation was detected byChIP-qPCR.Results1. After transfected with JARID1A siRNA48h, Ishikawa cell proliferation wasinhibited, the cells phase from G1to S phase was delay, and the G1phasewas stop(p<0.05). 2. The PR expression was up-regulated with siRNA, and down-regulated withpCMV-HA-JARID1A (p<0.05);The H3K4me3of PR gene promoter EREhalf-site was strengthen with siRNA in Ishikawa cells(p<0.05).Conclusion1. JARID1A siRNA through enhanced human endometrial cancer Ishikawacells PR gene， promoter ERE half-site H3K4me3level, restore PRexpression, inhibited endometrial cancer cell proliferation.2. The JARID1A gene is expected to be a new target for gene therapy ofendometrial cancer.