J Cancer 2020; 11(15):4453-4463. doi:10.7150/jca.44441

Research Paper

miR-223-5p targeting ERG inhibits prostate cancer cell proliferation and migration

Yongbao Wei1,2*, Junming Peng3*, Shuyun He4,5, Haijian Huang1,6, Le Lin1,2, Qingguo Zhu1,2, Liefu Ye1,2, Tao Li1,2, Xing Zhang7, Yunliang Gao4✉, Xiaochun Zheng1,8✉

1. Shengli Clinical Medical College of Fujian Medical University, Fuzhou 350001, China
2. Department of Urology, Fujian Provincial Hospital, Fuzhou 350001, China
3. Department of Urology, Shenzhen People's Hospital, Second Clinic Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen 518020, P.R. China.
4. Department of Urology, the Second Xiangya Hospital, Central South University, No139. Renmin Road, Changsha 410011, China
5. Department of Urology, The People's Hospital of Xiangtan Country, Xiangtan, China
6. Department of Pathology, Fujian Provincial Hospital, Fuzhou 350001, China
7. Department of Urology, the Traditional Chinese Medicine Hospital of Yangzhou, Yangzhou University of Traditional Chinese Medicine, Yangzhou, Jiangsu 225002, China
8. Department of Anesthesiology, Fujian Provincial Hospital, Fuzhou 350001, China.
* Contributed equally

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Citation:
Wei Y, Peng J, He S, Huang H, Lin L, Zhu Q, Ye L, Li T, Zhang X, Gao Y, Zheng X. miR-223-5p targeting ERG inhibits prostate cancer cell proliferation and migration. J Cancer 2020; 11(15):4453-4463. doi:10.7150/jca.44441. Available from http://www.jcancer.org/v11p4453.htm

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Abstract

Ectopic expression of miR-223-5p, the lagging strand of miR-223 duplex, has been reported acting as anti-tumor miRNA in many cancers. How miR-223-5p influencing prostate cancer (PCa) remains obscure and worth of experimental investigation. In this study, the expressions of miR-223-5p and ERG in common PCa cell lines were detected and compared to RWPE-1, respectively. Then luciferase reporter assay was performed to verify whether miR-223-5p could specifically target and regulate ERG. Further discovery ERG's role in the PCa oncogenesis was also conducted by up or down regulating miR-223-3p expression. We found miR-223-5p was significantly down-regulated in DU145, while it was only up-regulated in LNCaP. Similarly, ERG expression remarkably decreased in both PC-3 and DU145 than that in RWPE-1, but significantly increasing in LNCaP. Luciferase assay demonstrated slightly decreased ERG expression after miR-223-5p-mimics but significantly increased ERG expression after miR-223-5p-inhibtor. Using gene interference, we further confirmed that both ERG mRNA and protein expressions were decreased in all PCa lines transfected ERG siRNA, but increasing in both DU145 and LNCaP cells with miR-223-5p antisense oligonucleotides. MTT assay, Transwell invasion and migration assay supported the function of ERG in PCa oncogenesis. We revealed tumor suppressive abilities of miR-223-5p in PCa by negatively targeting ERG gene. It could serve as a fundamental supplement and extension of our previous study about miR-223-3p in PCa, revealing the coordinative regulation between miR-223-5p and miR-223-3p in PCa cell biological behaviors. Exploration of miR-233-duplex orientated pathway networks may help us develop novel potential therapeutic options for PCa.

Keywords: miR-223-5p, prostate cancer, ERG, biological behavior