长链非编码 RNA PCAT-1 通过 miR-145-5p 调控 FSCN1 促进前列腺癌的发生。
Long non-coding RNA PCAT-1 contributes to tumorigenesis by regulating FSCN1 via miR-145-5p in prostate cancer.
机构信息
Department of Urology, Huaihe Hospital of Henan University, Kaifeng, 475000, China.
Department of Urology, Huaihe Hospital of Henan University, Kaifeng, 475000, China.
出版信息
Biomed Pharmacother. 2017 Nov;95:1112-1118. doi: 10.1016/j.biopha.2017.09.019. Epub 2017 Oct 6.
Prostate cancer associated lncRNA transcript 1 (PCAT-1) has been identified as an oncogenic long non-coding RNA (lncRNA) in some solid tumors, including prostate cancer (PC). However, the molecular mechanism of PCAT-1 involved in PC is poorly defined. In this study, we found that PCAT-1 expression was up-regulated and miR-145-5p expression was down-regulated in PC tissues and cells. Function analysis indicated that PCAT-1 overexpression promoted proliferation, migration, invasion and inhibited apoptosis of PC cells. Rescue experiments demonstrated that miR-145-5p restoration attenuated the promotive effects of PCAT1 on PC progression, while Fascin-1 (FSCN1) upregulation relieved the anti-cancer role of miR-145-5p in PC. Mechanical analysis discovered that PCAT-1 could act as a miR-145-5p sponge to modulate FSCN1 expression. In conclusion, these findings suggested that PCAT-1 accelerated PC cell proliferation, migration, invasion and suppressed apoptosis by up-regulating FSCN1 mediated via miR-145-5p, hinting a potential therapeutic strategy for PC patients.
前列腺癌相关长链非编码 RNA 转录本 1（PCAT-1）已被确定为某些实体肿瘤中的致癌长链非编码 RNA（lncRNA），包括前列腺癌（PC）。然而，PCAT-1 参与 PC 的分子机制尚未明确。在本研究中，我们发现 PCAT-1 在 PC 组织和细胞中表达上调，miR-145-5p 表达下调。功能分析表明，PCAT-1 过表达促进 PC 细胞的增殖、迁移、侵袭，并抑制细胞凋亡。挽救实验表明，miR-145-5p 恢复减弱了 PCAT1 对 PC 进展的促进作用，而 Fascin-1（FSCN1）的上调减轻了 miR-145-5p 在 PC 中的抗癌作用。力学分析发现 PCAT-1 可以作为 miR-145-5p 的海绵体来调节 FSCN1 的表达。总之，这些发现表明，PCAT-1 通过上调 FSCN1 加速 PC 细胞的增殖、迁移、侵袭并抑制细胞凋亡，这提示了针对 PC 患者的潜在治疗策略。
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