lncRNA PTAR promotes NSCLC cell proliferation, migration and invasion by sponging microRNA-101
lncRNA PTAR promotes NSCLC cell proliferation, migration and invasion by sponging microRNA-101
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lncRNA PTAR 通过海绵 microRNA-101 促进 NSCLC 细胞增殖、迁移和侵袭
DOI：
10.3892/mmr.2019.10646
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发表时间：
2019-11-01
影响因子：
3.4
通讯作者：
Yao, Ruyong
中科院分区：
文献类型：
--
作者：
Yu, Wenjun;Sun, Zhenni;Yao, Ruyong
MicroRNA (miR)-101拷贝丢失是人类肺癌发展的早期事件，在所有肺癌发病率中占29%。此外，已知miR-101在非小细胞肺癌（NSCLC）中的表达下调。本研究的目的是探讨长链非编码RNA (lnc)-RNA促转化相关RNA （PTAR）在与miR-101相关的非小细胞肺癌细胞增殖、迁移和侵袭中的作用和机制。逆转录-定量PCR检测lncRNA PTAR在30对人NSCLC组织及相应肿瘤旁组织中的表达。将PTAR扩增并克隆到表达载体pCDNA3.1中。然后将ptar过表达质粒或小干扰(si)-RNA-PTAR转染A549细胞48 h，观察细胞增殖和细胞周期分布。此外，采用Transwell室法和细胞划伤法分析A549细胞的迁移和侵袭。评估荧光素酶活性测定以确定PTAR和miR-101之间的相互作用。此外，我们的研究结果表明，在人NSCLC组织和细胞系中，lncRNA PTAR的表达分别比正常肺组织和细胞系上调。此外，转染PTAR可促进A549细胞增殖、迁移和侵袭；siRNA-PTAR转染观察到相反的作用。荧光素酶活性测定显示PTAR可以作为海绵结合miR-101。因此，miR-101在NSCLC肿瘤发生和进展中发挥作用。综上所述，lncRNA PTAR通过海绵和失活miR-101来促进NSCLC细胞生长，这可能是人类NSCLC中miR-101拷贝丢失的可能机制。
MicroRNA (miR)-101 copy loss is an early event in the development of human lung cancer, and it occurs in 29% of all lung cancer incidences. In addition, miR-101 expression in non-small cell lung cancer (NSCLC) is known to be downregulated. The aim of the present study was to explore the roles and mechanisms of the long non-coding (lnc)-RNA pro-transition associated RNA (PTAR) on NSCLC cell proliferation, migration and invasion in association with miR-101. Reverse transcription-quantitative PCR analysis was performed to detect the expression of lncRNA PTAR in 30 paired human NSCLC tissues and the corresponding para-tumor tissues. PTAR was amplified and cloned into the expression vector pCDNA3.1. Then, PTAR-overexpression plasmids or small interfering (si)-RNA-PTAR was transfected into A549 cells for 48 h, after which cell proliferation and the cell cycle distribution were evaluated. In addition, Transwell chamber and cell scratch-wound assays were conducted to analyze A549 cell migration and invasion. A luciferase activity assay was evaluated to determine the interaction between PTAR and miR-101. Furthermore, our results demonstrated that in human NSCLC tissues and cell lines, lncRNA PTAR expression was upregulated compared with normal lung tissues and cell lines, respectively. Additionally, PTAR transfection was observed to promote A549 cell proliferation, migration and invasion; opposing effects were observed with siRNA-PTAR transfection. The luciferase activity assay revealed that PTAR could act as a sponge to bind miR-101. Thus, miR-101 plays a role in NSCLC tumorigenesis and progression. In conclusion, lncRNA PTAR was proposed to promote NSCLC cell growth through sponging and inactivating miR-101, which may be a possible mechanism underlying miR-101 copy loss in human NSCLC.