Long non-coding RNA PCAT-1 contributes to tumorigenesis by regulating FSCN1 via miR-145-5p in prostate cancer

被引:80
作者
Xu, Weibo [1 ]
Chang, Junkai [1 ]
Du, Xinyi [1 ]
Hou, Junqing [1 ]
机构
[1] Henan Univ, Dept Urol, Huaihe Hosp, 8 Baobei Rd, Kaifeng 475000, Peoples R China
关键词
Prostate cancer; lncRNA PCAT-1; miR-145-5p; FSCN1; CELL-PROLIFERATION; TUMOR-SUPPRESSOR; TARGETS; MIGRATION; PROSPECTS;
D O I
10.1016/j.biopha.2017.09.019
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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.
引用
收藏
页码:1112 / 1118
页数:7
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