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Cav-1通过长链非编码RNA HOTAIR促进肺癌细胞增殖和侵袭。

Cav-1 promote lung cancer cell proliferation and invasion through lncRNA HOTAIR.

作者信息

Liu Wei, Yin Nan-Chang, Liu Hao, Nan Ke-Jun

机构信息

Department of Oncology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China; Department of Oncology, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning, China.

Department of Thoracic Surgery, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning, China.

出版信息

Gene. 2018 Jan 30;641:335-340. doi: 10.1016/j.gene.2017.10.070. Epub 2017 Nov 6.

DOI:10.1016/j.gene.2017.10.070
PMID:29080835
Abstract

OBJECTIVES

Lung cancer is one of the most common malignant tumors worldwide, and its morbidity and mortality rates continue to rise. The role of lncRNAs in lung cancer has become an emerging area of research.

MATERIALS AND METHODS

The expression of CAV-1 and HOTAIR was determined in lung cancer tissues and cell lines by western blot and RT-qPCR. Cell proliferation, migration and invasion were analysed in lung cell following knockdown or overexpression of CAV-1 or HOTAIR by transfection with small interfering RNA (siRNA) or plasmid.

RESULTS

The expression of CAV-1 and HOTAIR in lung cancer tissues and cell lines was higher than in normal lung tissue or normal lung cell lines. We discovered that CAV-1 could regulate cell proliferation, migration and invasion. At the same time, CAV-1 could regulate the expression of HOTAIR. In addition, knockdown of the expression of HOAIR partially reverses the promotion of cell viability and invasion induced by CAV-1.

CONCLUSIONS

Our results indicated that CAV-1 coordinate the lung cancer through HOTAIR. And HOTAIR may become a novel target for lung cancer therapy.

摘要

目的

肺癌是全球最常见的恶性肿瘤之一,其发病率和死亡率持续上升。长链非编码RNA(lncRNAs)在肺癌中的作用已成为一个新兴的研究领域。

材料与方法

采用蛋白质免疫印迹法(western blot)和逆转录定量聚合酶链反应(RT-qPCR)检测肺癌组织及细胞系中CAV-1和HOTAIR的表达。通过转染小干扰RNA(siRNA)或质粒敲低或过表达CAV-1或HOTAIR后,分析肺细胞的增殖、迁移和侵袭情况。

结果

肺癌组织及细胞系中CAV-1和HOTAIR的表达高于正常肺组织或正常肺细胞系。我们发现CAV-1可调节细胞增殖、迁移和侵袭。同时,CAV-1可调节HOTAIR的表达。此外,敲低HOAIR的表达可部分逆转CAV-1对细胞活力和侵袭的促进作用。

结论

我们的结果表明,CAV-1通过HOTAIR协同作用于肺癌。并且HOTAIR可能成为肺癌治疗的新靶点。

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