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Research Paper|Volume 13, Issue 14|pp 18527—18544

LncRNA CCAT1 promotes prostate cancer cells proliferation, migration, and invasion through regulation of miR-490-3p/FRAT1 axis

Xiaowei Cai1, Yiheng Dai2, Peng Gao1, Guanyu Ren3, Dingcai Cheng4, Bo Wang2, Yi Wang2, Jiang Yu2, Yiheng Du2, Xizhi Wang2, Boxin Xue1
  • 1Department of Urology, Second Affiliated Hospital of Soochow University, Suzhou 215004, Jiangsu, China
  • 2Department of Urology, Suzhou Kowloon Hospital Shanghai Jiao Tong University School of Medicine, Suzhou 215021, Jiangsu, China
  • 3Department of Urology, Changhai Hospital, Naval Medical University, Shanghai 200433, Yangpu, China
  • 4Department of Urology, Taixing People's Hospital, Taixing 225400, Jiangsu, China
* Equal contribution
Received: September 29, 2020Accepted: April 29, 2021Published: July 28, 2021
https://doi.org/10.18632/aging.203300

Copyright: © 2021 Cai 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

Prostate cancer (PCa) is a prevalent cancer in males, with high incidence and mortality. Recent studies have shown the crucial role of long non-coding RNA (lncRNA) in PCa. Here, we aimed to explore the functional roles and inner mechanisms of lncRNA CCAT1 in PCa cells. qRT-PCR results showed that CCAT1 was upregulated in PCa tissues and cells. Functional assays demonstrated that CCAT1 knockdown suppressed cell proliferation, migration, invasion, yet promoted apoptosis, while CCAT1 promotion showed the opposite results. We also found that CCAT1 negatively regulated miR-490-3p expression and subsequently regulated FRAT1 expression. Inhibition of miR-490-3p or up-regulation of FRAT1 reversed the suppressive effects of CCAT1 knockdown on the PCa cells. In conclusion, CCAT1 regulated FRAT1 expression through miR-490-3p and then promote the PCa cells proliferation, migration, and invasion, which reveals the oncogenic function of CCAT1 in PCa progress.