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miR-615 Inhibits Prostate Cancer Cell Proliferation and Invasion by Directly Targeting Cyclin D2

Fengyu Huang*†, Hongjun Zhao, Zhaojin Du, Hong Jiang§

* Qingdao University, Qingdao, P.R. China
† Department of Urology, Yantai Municipal Laiyang Central Hospital, Laiyang, Shandong Province, P.R. China
‡ Reproductive Medical Center, Qingdao Women and Children’s Hospital, Qingdao University, Qingdao, Shandong Province, P.R. China
§ Department of Gastroenterology, Yantai Municipal Laiyang Central Hospital, Laiyang, Shandong Province, P.R. China

Oncology Research 2019, 27(3), 293-299. https://doi.org/10.3727/096504018X15190399381143

Abstract

Previous studies have reported that miR-615 exerts a tumor suppressor role in some tumors, such as esophageal squamous cell carcinoma and non-small cell lung cancer. However, the role of miR-615 in prostate cancer has not been defined. Here we found that miR-615 was downregulated in prostate cancer tissues and cell lines. Overexpression of miR-615 in PC-3 cells significantly inhibited cellular proliferation, migration, and invasion. Moreover, overexpression of miR-615 delayed tumor growth in vivo. In terms of mechanism, we found that cyclin D2 (CCND2) is a target gene of miR-615 in prostate cancer. We showed that miR-615 could bind to the 3 -UTR region of CCND2 mRNA and inhibit its expression. There was a negative correlation between the expression of miR-615 and CCND2 in prostate cancer tissues. Moreover, restoration of cyclin D2 abolished the inhibitory effects of miR-615 on the proliferation, migration, and invasion of prostate cancer cells. Taken together, our study identified miR-615 as a tumor suppressor by targeting cyclin D2 in prostate cancer.

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Cite This Article

Huang, F., Zhao, H., Du, Z., Jiang, H. (2019). miR-615 Inhibits Prostate Cancer Cell Proliferation and Invasion by Directly Targeting Cyclin D2. Oncology Research, 27(3), 293–299.



cc This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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