Neoplasma Vol.67, No.4, p.825–833, 2020
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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 |
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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. 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.
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| Keywords: miR-193a-5p, HOXA7, proliferation, apoptosis, ovarian cancer |
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Published online: 16-Apr-2020
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| Year: 2020, Volume: 67, Issue: 4 |
Page From: 825, Page To: 833 |
doi:10.4149/neo_2020_190730N687
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