Yan-Hua L, Xiang-Lei L, Hong L, Jian-Jun W
Department of Oncology, Huaihe Hospital of Henan University, Kaifeng, China.
Indian J Cancer. 2015 Dec;52 Suppl 3:E190-3. doi: 10.4103/0019-509X.186579.
Long noncoding ribonucleic acids (RNAs) nowadays emerge as important biomarkers or potential therapeutic targets discussed in human cancers. Among them, maternally expressed gene 3 (MEG3) is known to be decreased in a variety of malignancies.
Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to detect the expression of MEG3 in forty pairs of lung cancer (LC) tissues. Overexpression of MEG3 was carried out, and we determined its effect on cell proliferation, apoptosis, and migration evaluated by cell counting kit-8, flow cytometric, and transwell analysis. Messenger RNA and protein expression of MYC were determined by qRT-PCR and western blot, respectively.
The expression of MEG3 was downregulated in LC tissues. Forced expression of MEG3 led to reduced abilities of cell proliferation and elevated apoptosis rate. It also slightly inhibited cell migration capacity in vitro. In addition, MYC was inhibited by MEG3 overexpression at both transcriptional and translational levels.
Our findings revealed MEG3 could regulate LC progression and serve as an important target for LC treatment.
长链非编码核糖核酸（RNA）如今已成为人类癌症中讨论的重要生物标志物或潜在治疗靶点。其中，母系表达基因3（MEG3）在多种恶性肿瘤中表达降低。
采用定量逆转录-聚合酶链反应（qRT-PCR）检测40对肺癌（LC）组织中MEG3的表达。进行MEG3过表达实验，并通过细胞计数试剂盒-8、流式细胞术和Transwell分析来确定其对细胞增殖、凋亡和迁移的影响。分别通过qRT-PCR和蛋白质印迹法测定MYC的信使RNA和蛋白质表达。
LC组织中MEG3表达下调。MEG3的强制表达导致细胞增殖能力降低和凋亡率升高。它在体外也轻微抑制细胞迁移能力。此外，MEG3过表达在转录和翻译水平均抑制MYC。
我们的研究结果表明MEG3可调节LC进展，并可作为LC治疗的重要靶点。
