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长链非编码RNA TUG1通过调控上皮性卵巢癌细胞中的AURKA促进细胞增殖并抑制细胞凋亡。

LncRNA TUG1 promotes cells proliferation and inhibits cells apoptosis through regulating AURKA in epithelial ovarian cancer cells.

作者信息

Li Tonghuai, Chen Yan, Zhang Jingjing, Liu Shaoxiao

机构信息

Department of Gynaecology and Obstetrics Department of Imaging, People's Hospital of Lishui City, the Sixth Affiliated Hospital of Wenzhou Medical University, Lishui, China.

出版信息

Medicine (Baltimore). 2018 Sep;97(36):e12131. doi: 10.1097/MD.0000000000012131.

Abstract

This study aimed to assess the effect of long noncoding RNAs (lncRNAs) taurine-upregulated gene 1 (TUG1) on cells proliferation and apoptosis as well as its targeting genes in epithelial ovarian cancer (EOC) cells.Blank mimic, lncRNA TUG1 mimic, blank inhibitor, and lncRNA TUG1 inhibitor plasmids were transfected into SK-OV-3 (SKOV3) cells. Rescue experiment was performed by the transfection of lncRNA TUG1 inhibitor and Aurora kinase A (AURKA) mimic plasmids into SKOV3 cells. Cell counting kit-8 (CKK-8), annexin V-FITC (AV)-propidium iodide (PI) (AV-PI), quantitative polymerase chain reaction (qPCR), and western blot assays were performed to detect cells proliferation, apoptosis, RNA expression, and protein expression respectively.Cells proliferation was increased in lncRNA TUG1 mimic group and decreased in lncRNA TUG1 inhibitor group than normal control (NC) groups. Cells apoptosis rate was repressed after treatment with lncRNA TUG1 mimic and promoted after treatment with lncRNA TUG1 inhibitor. AURKA expression but not CLDN3, SERPINE1, or ETS1 expression was adversely regulated by lncRNA TUG1 mimic and inhibitor. After transferring lncRNA TUG1 (-) and AURKA (+) plasmids, cells proliferation was increased, while cells apoptosis rate was decreased in AURKA mimic (+)/lncRNA TUG1 inhibitor (-) group than NC (+)/lncRNA TUG1 (-) group, which suggested lncRNA TUG1 regulated cells proliferation and cells apoptosis through targeting AURKA.LncRNA TUG1 promotes cells proliferation and inhibits cells apoptosis through regulating AURKA in EOC cells.

摘要

本研究旨在评估长链非编码RNA(lncRNA)牛磺酸上调基因1(TUG1)对上皮性卵巢癌(EOC)细胞增殖和凋亡的影响及其靶向基因。将空白模拟物、lncRNA TUG1模拟物、空白抑制剂和lncRNA TUG1抑制剂质粒转染至SK-OV-3(SKOV3)细胞中。通过将lncRNA TUG1抑制剂和极光激酶A(AURKA)模拟物质粒转染至SKOV3细胞中进行挽救实验。分别采用细胞计数试剂盒-8(CKK-8)、膜联蛋白V-异硫氰酸荧光素(AV)-碘化丙啶(PI)(AV-PI)、定量聚合酶链反应(qPCR)和蛋白质印迹分析来检测细胞增殖、凋亡、RNA表达和蛋白质表达。与正常对照(NC)组相比,lncRNA TUG1模拟物组细胞增殖增加,lncRNA TUG1抑制剂组细胞增殖减少。用lncRNA TUG1模拟物处理后细胞凋亡率受到抑制,用lncRNA TUG1抑制剂处理后细胞凋亡率升高。lncRNA TUG1模拟物和抑制剂对AURKA表达有负向调节作用,但对紧密连接蛋白3(CLDN3)、丝氨酸蛋白酶抑制剂E1(SERPINE1)或ETS1转录因子(ETS1)表达无影响。转染lncRNA TUG1(-)和AURKA(+)质粒后,与NC(+)/lncRNA TUG1(-)组相比,AURKA模拟物(+)/lncRNA TUG1抑制剂(-)组细胞增殖增加,细胞凋亡率降低,这表明lncRNA TUG1通过靶向AURKA调节细胞增殖和细胞凋亡。在EOC细胞中,lncRNA TUG1通过调节AURKA促进细胞增殖并抑制细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d2e/6133603/fee223550d94/medi-97-e12131-g002.jpg

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