Summary: | Fan Shi, Tao Wang, Zi Liu, Yingbing Zhang, Juan Wang, Kaishuo Zhang, Jin Su Department of Radiation Oncology, First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi Province 710061, People’s Republic of ChinaCorrespondence: Fan ShiDepartment of Radiation Oncology, First Affiliated Hospital of Xi’an Jiaotong University, No.277 Yanta West Road, Xi’an, Shaanxi Province 710061, People’s Republic of ChinaTel +86 29 8532 4019Email xdogheqhyrf55@163.comIntroduction: MiR143HG is a recently identified tumor suppressor in bladder cancer. We performed bioinformatics prediction and found that miR143HG can form base pairs with miR-125a. This study was therefore carried out to explore the interaction between miR143HG and miR-125a in endometrial carcinoma (EC).Methods: Gene expression was analyzed by qPCR and Western blot. Interactions among genes were analyzed by over-expression experiments. Cell apoptosis after transfections was analyzed by cell apoptosis assay.Results: We found that the down-regulation of miR143HG in EC predicted poor survival. Bioinformatics analysis showed that miR-125a could bind miR143HG. In EC tissues, miR143HG was positively correlated with p53, not miR-125a. In EC cells, miR143HG and miR-125a over-expression failed to affect the expression of each other. However, miR143HG over-expression led to the up-regulated p53. MiR-125a over-expression played the opposite role and attenuated the effects of miR143HG over-expression. Cell apoptosis analysis showed that miR143HG and p53 over-expression led to an increased cell apoptotic rate. MiR-125a over-expression played the opposite role and attenuated the effects of miR143HG over-expression.Conclusion: MiR143HG may up-regulate p53 in EC by sponging miR-125a to promote cancer cell apoptosis.Keywords: miR143HG, endometrial carcinoma, miR-125a, p53
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