MicroRNA-200a promotes proliferation and invasion of ovarian cancer cells by targeting PTEN

J.-H. Jiang, Q.-Y. Lv, Y.-X. Yi, J. Liao, X.-W. Wang, W. Zhang

Department of Gynecology, Zhongnan Hospital of Wuhan University, Wuhan, China. zw6676@163.com

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• Oncology

OBJECTIVE: We investigate whether microRNA-200a could regulate proliferation and invasion of ovarian cancer cells, thereby participating in the occurrence and development of ovarian cancer. We also explore the specific mechanism of microRNA-200a in regulating ovarian cancer.

PATIENTS AND METHODS: Expression level of microRNA-200a in ovarian cancer tissues and paracancerous tissues were detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The regulatory effects of microRNA-200a on proliferation and invasion of ovarian cancer cells were examined by Cell counting kit-8 (CCK-8) and cell invasion assay, respectively. Dual-luciferase reporter gene assay was performed to confirm the binding relationship between microRNA-200a and PTEN (phosphatase and tensin homolog deleted on chromosome ten). The regulatory role of microRNA-200a in PTEN expression was accessed by Western blot. Rescue experiments were conducted to assess whether microRNA-200a regulated proliferation and invasion of ovarian cancer cells by inhibiting PTEN expression.

RESULTS: MicroRNA-200a expression in ovarian cancer tissues was significantly higher than that of paracancerous tissues. Besides, microRNA-200a was also overexpressed in ovarian cancer cell lines than that of normal ovarian cells. Overexpression of microRNA-200a promoted the proliferative and invasive abilities of SKOV3 and OVCAR3 cells. Dual-luciferase reporter gene assay showed that microRNA-200a could directly degrade PTEN. Overexpression of PTEN in SKOV3 and OVCAR3 cells partially reversed the increased cell proliferation and invasion induced by overexpressed microRNA-200a.

CONCLUSIONS: Overexpressed microRNA-200a promoted the proliferative and invasive abilities of ovarian cancer cells, which might be related to the targeted regulation of PTEN expression.

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