Department of Urology, Second Affiliated Hospital of Soochow University, Suzhou 215004, Jiangsu, China.
Department of Urology, Suzhou Kowloon Hospital Shanghai Jiao Tong University School of Medicine, Suzhou 215021, Jiangsu, China.
Aging (Albany NY). 2021 Jul 28;13(14):18527-18544. doi: 10.18632/aging.203300.
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.
前列腺癌(PCa)是男性中常见的癌症,发病率和死亡率都很高。最近的研究表明,长链非编码 RNA(lncRNA)在 PCa 中起着关键作用。在这里,我们旨在探讨 lncRNA CCAT1 在 PCa 细胞中的功能作用和内在机制。qRT-PCR 结果表明,CCAT1 在 PCa 组织和细胞中上调。功能测定表明,CCAT1 敲低抑制细胞增殖、迁移和侵袭,但促进细胞凋亡,而 CCAT1 促进则表现出相反的结果。我们还发现,CCAT1 负调控 miR-490-3p 的表达,进而调控 FRAT1 的表达。抑制 miR-490-3p 或上调 FRAT1 逆转了 CCAT1 敲低对 PCa 细胞的抑制作用。总之,CCAT1 通过 miR-490-3p 调节 FRAT1 的表达,从而促进 PCa 细胞的增殖、迁移和侵袭,这揭示了 CCAT1 在 PCa 进展中的致癌作用。