LncRNA TUG1 promotes cells proliferation and inhibits cells apoptosis through regulating AURKA in epithelial ovarian cancer cells.
LncRNA TUG1 promotes cells proliferation and inhibits cells apoptosis through regulating AURKA in epithelial ovarian cancer cells.
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DOI：
10.1097/md.0000000000012131
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发表时间：
2018-09
期刊：
影响因子：
1.6
通讯作者：
Liu S
中科院分区：
文献类型：
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作者：
Li T;Chen Y;Zhang J;Liu S
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) 模拟质粒转染至 SKOV3 细胞中进行拯救实验。细胞计数试剂盒8（CKK-8）、膜联蛋白V-FITC（AV）-碘化丙啶（PI）（AV-PI）、定量聚合酶链反应（qPCR）和蛋白质印迹法分别检测细胞增殖、凋亡、RNA表达和蛋白表达。与正常对照组（NC）组相比，lncRNA TUG1模拟组的细胞增殖增加，而lncRNA TUG1抑制剂组的细胞增殖减少。 lncRNA TUG1模拟物处理后细胞凋亡率受到抑制，而lncRNA TUG1抑制剂处理后细胞凋亡率得到促进。 lncRNA TUG1 模拟物和抑制剂对 AURKA 表达产生不利调节，但 CLDN3、SERPINE1 或 ETS1 表达不受抑制。转入lncRNA TUG1（−）和AURKA（+）质粒后，AURKA模拟（+）/lncRNA TUG1抑制剂（−）组细胞增殖增加，细胞凋亡率低于NC（+）/lncRNA TUG1（−）组，提示lncRNA TUG1通过靶向AURKA调节细胞增殖和细胞凋亡。 LncRNA TUG1通过调节EOC细胞中的AURKA促进细胞增殖并抑制细胞凋亡。
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.