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Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

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Title: MiR-193a-5p suppresses cell proliferation and induces cell apoptosis by regulating HOXA7 in human ovarian cancer.
Author: S. WANG, Y.J. DIAO, B.B. ZHU

Abstract: Ovarian cancer is one of the most common malignancies in women in the world. MicroRNAs (miRNAs) were identified as a group of regulators that played important roles in the progression of cancer development. The main purpose of this study was to investigate the functional mechanism of microRNA-193a-5p (miR-193a-5p) in human ovarian cancer. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the RNA levels of miR-193a-5p and homeobox genes A7 (HOXA7). Western blot assay was performed to determine the protein level of HOXA7. The interaction between miR-193a-5p and HOXA7 was predicted by online software starBase v3.0, and then verified by the dual luciferase reporter assay. The cell proliferation and apoptosis rate were examined by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) and colony formation assay as well as flow cytometry analysis, respectively. We found out that the expression level of miR-193a-5p was decreased in human ovarian cancer tissues and cells. The overexpression of miR-193a-5p inhibited cell proliferation and induced apoptosis in human ovarian cancer. Interestingly, miR-193a-5p reduced the expression of HOXA7 by binding to 3’-untranslated region (3’-UTR) of HOXA7 mRNA. As expected, the knockdown of HOXA7 also suppressed cell proliferation and promoted apoptosis in human ovarian cancer. Besides, the upregulation of HOXA7 reversed the effect of miR-193a-5p on human ovarian cell proliferation and apoptosis. Our findings confirmed that miR-193a-5p inhibited cell proliferation and induced apoptosis through the downregulation of HOXA7 in human ovarian cancer, providing a theoretical value for the therapy of human ovarian cancer.

Keywords: miR-193a-5p, HOXA7, proliferation, apoptosis, ovarian cancer
Published online: 16-Apr-2020
Year: , Volume: , Issue: Page From: , Page To:

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