MicroRNA-214 Suppresses Ovarian Cancer by Targeting β-Catenin

Background/Aims: Ovarian cancer is one of the most common malignancies with a high rate of mortality in women. However, current therapies for ovarian cancer treatment are ineffective. Therefore, novel target identification is an urgent requisite. The present study aimed to investigate the role of mi...

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Bibliographic Details
Main Authors: Yang Liu, Jie Lin, Shujuan Zhai, Chunyi Sun, Changjun Xu, Honglin Zhou, Huijin Liu
Format: Article
Language:English
Published: Cell Physiol Biochem Press GmbH & Co KG 2018-02-01
Series:Cellular Physiology and Biochemistry
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Online Access:https://www.karger.com/Article/FullText/487733
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Summary:Background/Aims: Ovarian cancer is one of the most common malignancies with a high rate of mortality in women. However, current therapies for ovarian cancer treatment are ineffective. Therefore, novel target identification is an urgent requisite. The present study aimed to investigate the role of microRNA-214 (miR-214) in ovarian cancer. Methods: The expression of miR-214, β-catenin, cyclin D1, c-myc, and TCF-1 at the transcriptional level was measured by real-time PCR, while that of β-catenin, Cyclin D1, and c-Myc at the protein level were detected by western blot. Colony formation assay and transwell assay were used to explore the invasion ability of the cancer cells. Cell cycle was measured by flow cytometry. Results: Real-time PCR showed that miR-214 expression in ovarian cancer cell lines was lower than that in the human normal ovarian epithelial cells, IOSE80. Furthermore, the low expression of miR-214 was correlated with high pathological grade. The rate of colony formation and invasion of miR-214 overexpression in SKOV-3 cells were weaker than that in control cells. Moreover, miR-214 overexpression led to the G0/G1 phase arrest. The expression of β-catenin, Cyclin D1, and c-Myc was suppressed by the overexpression of miR-214. Conclusion: These results suggested that miR-214 may serve as a tumor suppressor of ovarian cancer by targeting the β-catenin pathway.
ISSN:1015-8987
1421-9778