长链非编码RNA MIR210HG通过直接调控miR-874/STAT3轴促进非小细胞肺癌进展。
LncRNA MIR210HG Facilitates Non-Small Cell Lung Cancer Progression Through Directly Regulation of miR-874/STAT3 Axis.
作者信息
Bu Liang, Zhang Libin, Tian Mei, Zheng Zhoubin, Tang Huijie, Yang Qiuju
机构信息
The First People's Hospital of Yunnan Province, Medical School of Kunming University of Science and Technology, Kunming, China.
Anesthesiology Department, No.1 People's General Hospital of Yunnan Province, Kunming, Yunnan, China.
出版信息
Dose Response. 2020 Jul 10;18(3):1559325820918052. doi: 10.1177/1559325820918052. eCollection 2020 Jul-Sep.
BACKGROUND
Long noncoding RNAs are involved in the progression of multiple cancers. However, the expression and mechanism of microRNA (miR)210HG in non-small cell lung cancer (NSCLC) remain unclear.
METHODS
The levels of miR210HG and miR-874 were measured by quantitative real-time polymerase chain reaction in NSCLC tissue samples and cells. Non-small cell lung cancer cell proliferation, migration, and invasion were measured by Cell Counting Kit-8 and transwell assays. Luciferase analysis confirmed the interaction between miR210HG and miR-874.
RESULTS
Here, our data showed that miR210HG was overexpressed in NSCLC tissue samples and cells. In vitro functional assays showed that silencing miR210HG blocked NSCLC cell proliferation, migration, and invasion while promoting NSCLC cell radiosensitivity and chemoresistance. Mechanistically, miR-874 was directly regulated by miR210HG. Furthermore, miR-874 expression was reduced in NSCLC tissues and cells. The miR-874 mimic could mitigate the promoting effect of miR210HG on NSCLC cell progression. The data also showed that miR210HG promoted NSCLC cell progression through miR-181a expression by targeting STAT3.
CONCLUSIONS
Our observations suggest that miR210HG is associated with NSCLC cell progression by regulating the miR-874/STAT3 axis.
背景
长链非编码RNA参与多种癌症的进展。然而，微小RNA（miR）210HG在非小细胞肺癌（NSCLC）中的表达及机制仍不清楚。
方法
采用定量实时聚合酶链反应检测NSCLC组织样本和细胞中miR210HG和miR - 874的水平。通过细胞计数试剂盒 - 8和Transwell实验检测非小细胞肺癌细胞的增殖、迁移和侵袭能力。荧光素酶分析证实miR210HG与miR - 874之间的相互作用。
结果
我们的数据显示，miR210HG在NSCLC组织样本和细胞中过表达。体外功能实验表明，沉默miR210HG可阻断NSCLC细胞的增殖、迁移和侵袭，同时提高NSCLC细胞的放射敏感性和化学抗性。机制上，miR - 874受miR210HG直接调控。此外，NSCLC组织和细胞中miR - 874表达降低。miR - 874模拟物可减轻miR210HG对NSCLC细胞进展的促进作用。数据还表明，miR210HG通过靶向STAT3促进miR - 181a表达，从而促进NSCLC细胞进展。
结论
我们的观察结果表明，miR210HG通过调节miR - 874/STAT3轴与NSCLC细胞进展相关。
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