Over-expression of miR-1271 inhibits endometrial cancer cells proliferation and induces cell apoptosis by targeting CDK1

L. Li, Y.-W. Qu, Y.-P. Li

Maternal and Child Care Service Centre of Kuiwen District, Weifang, Shandong, China. ppy9009@yeah.net

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• Oncology

OBJECTIVE: Endometrial carcinoma (EC) is one of the most common female malignancies worldwide. Growing evidence showed that microRNAs (miRNAs) are involved in the EC progression. The present study aimed to investigate the role of miR-1271 in the development and progression of EC.

PATIENTS AND METHODS: The EC tissues and adjacent normal tissues were obtained from 42 EC patients. The expression of miR-1271 in EC tissues and cells was examined using Real-time RT-PCR. Western blot was used to quantify the level of cyclin-dependent kinase 1 (CDK1) in EC tissues and cells lines. Cell proliferation, colony formation and flow cytometry were done to examine effects on cancer cell proliferation and apoptosis in vitro. Bioinformatics software was used to predict some potential target genes of miR-1271. Besides, the dual luciferase reporter gene assay was used to determine the direct targeting relationship between miR-1271 and CDK1.

RESULTS: MiR-1271 was significantly downregulated in human EC tissues and cells while CDK1 was strongly upregulated. Bioinformatics analysis indicated that CDK1 was a potential target of miR-1271. Then, luciferase reporter assay confirmed that CDK1 was a direct target gene of miR-1271. In vitro studies showed that miR-1271 overexpression reduced EC cell proliferation and promoted apoptosis, while restoration of CDK1 attenuated these effects of miR-1271 on EC cells. Moreover, we found that knockdown of miR-1271 significantly promoted EC cell growth and suppressed apoptosis.

CONCLUSIONS: Our findings showed that miR-1271 served as a tumor suppressor in EC via targeting CDK1, suggesting miR-1271 as a new potential target for therapy strategy in EC.

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