Research Paper Volume 12, Issue 10 pp 8880—8892
lncRNA OGFRP1 functions as a ceRNA to promote the progression of prostate cancer by regulating SARM1 level via miR-124-3p
- 1 Department of Urology, QiLu Hospital of Shandong University, Jinan 250012, Shandong, P.R. China
- 2 Department of Gynecology, Jinan Central Hospital, Jinan 250012, Shandong, P.R. China
- 3 Pathology Department, Basic Medical School, Shandong University, Jinan 250012, Shandong, P.R. China
- 4 Department of Urology, Jinan Central Hospital Affiliated to Shandong First Medical University, Jinan 250012, Shandong, P.R. China
Received: November 20, 2019 Accepted: March 3, 2020 Published: May 19, 2020
https://doi.org/10.18632/aging.103007How to Cite
Copyright © 2020 Yan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
lncRNA can interact with miRNA as a ceRNA to participate in the regulation of target gene expression, thus playing an important role in the development of malignant tumors. In this research, we found that OGFRP1 was up-regulated in prostate cancer (PCa) clinical samples and cell lines. Additionally, OGFRP1 is significantly associated with TNM stages III and IV and perineural invasion. Knockdown of OGFRP1 inhibited the growth of PCa cells, suggesting a promotional effect of OGFRP1 in tumor progression. Interestingly, OGFRP1 primarily localized in the cytoplasm, while miR-124-3p was found to bind to OGFRP1. Therefore, we further analyzed the downstream target of miR-124-3p using TargetScan. The result of the luciferase reporter gene assay displayed that SARM1 was a downstream target of miR-124-3p in two PCa cell lines. The overexpression of SARM1 promoted growth and metastasis in PCa cells. Knockdown of OGFRP1 and overexpression of miR-124-3p markedly restored the promotion of SARM1 to PCa cells. In conclusion, lncRNA OGFRP1 completely bound to miR-124-3p and relieved their inhibition on SARM1, thus promoting the growth of PCa cells. This report extended our understanding of the underlying molecular mechanisms of lncRNAs in PCa, which could help us find novel diagnostic and therapeutic targets.