MiR-513a-3p inhibits EMT mediated by HOXB7 and promotes sensitivity to cisplatin in ovarian cancer cells
Y. Chen, X.-H. Zhao, D.-D. Zhang, Y. Zhao Department of Gynecology and Obstetrics, Ningbo Zhenhai Lianhua Hospital, Ningbo, China. zhaoyun6222@163.com
OBJECTIVE: Our aim was to investigate the biological function and mechanism of action of miR-513a-3p in ovarian cancer cells.
MATERIALS AND METHODS: In this study, qRT-PCR, Western blots, and immunohistochemistry experiments were among the methods used to examine the expression of miR-513a-3p, HOXB7, and related transcripts within ovarian cancer cells. An MTT assay was conducted to evaluate the viability of ovarian cancer cells in the presence of cisplatin. Transwell and wound-healing assays were performed to examine cell migration and invasion. Dual-Luciferase reporter assays were used to evaluate interactions among the aforementioned target genes. In vivo tumorigenesis experiments were conducted to verify biological effects of miR-513a-3p and HOXB7.
RESULTS: HOXB7 expression was relatively higher and MiR-513a-3p expression was relatively lower in ovarian cancer cells. Down-regulated expression of miR-513a-3p promoted cell movement via its ability to regulate epithelial-mesenchymal transition (EMT). Furthermore, decreased expression of miR-513a-3p resulted in increased sensitivity to cisplatin and resulted in poor prognosis in ovarian cancer patients who had relapsed after treatment with cisplatin. However, HOXB7 reversed the impact of miR-513a-3p in ovarian cancer cells. These results suggested that miR-513a-3p altered EMT mediated by HOXB7 and cisplatin-resistance.
CONCLUSIONS: MiR-513a-3p plays a critical role in promoting sensitivity to cisplatin and tumorigenesis via targeting HOXB7 in ovarian cancer.
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To cite this article
Y. Chen, X.-H. Zhao, D.-D. Zhang, Y. Zhao
MiR-513a-3p inhibits EMT mediated by HOXB7 and promotes sensitivity to cisplatin in ovarian cancer cells
Eur Rev Med Pharmacol Sci
Year: 2020
Vol. 24 - N. 20
Pages: 10391-10402
DOI: 10.26355/eurrev_202010_23389