Zhang Guanying, Han Guangye, Zhang Xinjun, Yu Quanfeng, Li Zeyu, Li Zhenhui, Li Jianchang
a The Second Department of Urinary Surgery , The First Affiliated Hospital of Xinxiang Medical University , Weihui , Henan , China.
b The First Department of Urinary Surgery , The First Affiliated Hospital of Xinxiang Medical University , Weihui , Henan , China.
Biomarkers. 2018 Jul;23(5):435-445. doi: 10.1080/1354750X.2018.1443509. Epub 2018 Mar 21.
Prostate cancer (PCa) is one of the most commonly diagnosed malignancy in men in the western world.
We aim to investigate the biological role of long non-coding RNA FENDRR and its mechanism in PCa.
We determined the expression of FENDRR and miR-18a-5p in PCa tissues and examined the regulatory mechanism in PCa cell lines.
FENDRR transcripts in human PCa tissues were significantly decreased compared with the normal controls. Reduced expression of FENDRR was correlated with the increase of pathological degree and poor prognosis in PCa patients. Upregulation of FENDRR inhibited cell proliferation, increased apoptosis and decreased invasion and migration ability, which was inhibited by miR-18a-5p mimic. Knockdown of FENDRR resulted in a significant increase of PCa cell proliferation and decrease of apoptosis and this effect was inhibited miR-18a-5p inhibitor. FENDRR and RUNX1 contain potential target sites for miR-18a-5p. miR-18a-5p mimic inhibited RUNX1 expression and luciferase activity. FENDRR could increase RUNX1 expression, which was inhibited by miR-18a-5p. The effect of FENDRR on cell proliferation, apoptosis and invasion and migration ability was suppressed by silence of RUNX1.
These results position FENDRR/miR-18a-5p/RUNX1 as a potential therapeutic target and biomarker for PCa.
前列腺癌（PCa）是西方世界男性中最常被诊断出的恶性肿瘤之一。
我们旨在研究长链非编码RNA FENDRR在前列腺癌中的生物学作用及其机制。
我们测定了前列腺癌组织中FENDRR和miR-18a-5p的表达，并在前列腺癌细胞系中研究了其调控机制。
与正常对照相比，人前列腺癌组织中的FENDRR转录本显著减少。FENDRR表达降低与前列腺癌患者病理程度增加和预后不良相关。FENDRR的上调抑制细胞增殖，增加细胞凋亡，并降低侵袭和迁移能力，而miR-18a-5p模拟物可抑制这种作用。敲低FENDRR导致前列腺癌细胞增殖显著增加，细胞凋亡减少，而miR-18a-5p抑制剂可抑制这种作用。FENDRR和RUNX1含有miR-18a-5p的潜在靶位点。miR-18a-5p模拟物抑制RUNX1表达和荧光素酶活性。FENDRR可增加RUNX1表达，而miR-18a-5p可抑制这种作用。RUNX1沉默可抑制FENDRR对细胞增殖、凋亡以及侵袭和迁移能力的影响。
这些结果表明FENDRR/miR-18a-5p/RUNX1是前列腺癌潜在的治疗靶点和生物标志物。
