4.2 Article

Upregulation of Long Noncoding RNA GAS5 Inhibits Lung Cancer Cell Proliferation and Metastasis via miR-205/PTEN Axis

期刊

MEDICAL SCIENCE MONITOR
卷 25, 期 -, 页码 2311-2319

出版社

INT SCIENTIFIC INFORMATION, INC
DOI: 10.12659/MSM.912581

关键词

Carcinoma, Non-Small-Cell Lung; MicroRNAs; PTEN Phosphohydrolase; RNA, Long Noncoding

资金

  1. National Natural Science Foundation of China (NSFC) [81672650]

向作者/读者索取更多资源

Background: Long noncoding RNA (lncRNA) is a key part of noncoding RNA class and increasing evidences have manifested that it plays a significant role in the physiology and pathology. The growth arrest-specific transcript 5 (GAS5) is a vital tumor suppressor in some types of cancers. However, the function of GAS5 in lung cancer remains largely no clear. The purpose of the current study was to identify the biological role of GAS5 in non-small cell lung cancer (NSCLC). Material/Methods: To study the role of GAS5 in the NSCLC, the RT-PCR, Western Blot, Luciferase assay, and RNA immunoprecipitation assay was employed to determine the relationship of GAS5, miR-205, and PTEN. CCK8 assay, Cell migration and invasion assay was used for the role of GAS5 in lung cancer cell proliferation and metastasis. Results: The results indicated that GAS5 was drastically downregulated in lung cancer cell lines. Further functional analysis showed that down-expression of GAS5 remarkably induced NSCLC growth, migration, and invasion. The luciferase reporter assays determined that miR-205 was a direct target of GAS5 in lung cancer. Moreover, the Phosphatase and tensin homologue (PTEN) was known as a direct target of miR-205 and miR-205/PTEN rescued the effects of GAS5 in NSCLC cells. Conclusions: To sum up, our results illustrate that upregulation of GAS5 in NSCLC suppresses its growth, migration, and invasion via the miR-205/PTEN axis.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.2
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据