PTEN公司
煤气5
下调和上调
长非编码RNA
癌症研究
小RNA
转移
细胞生长
小核仁RNA
竞争性内源性RNA
非编码RNA
肺癌
生物
医学
肿瘤科
内科学
癌症
PI3K/AKT/mTOR通路
细胞生物学
基因
信号转导
遗传学
作者
Lizhen Dong,Guangming Li,Yongmei Li,Ziyang Zhu
出处
期刊:Medical Science Monitor
[International Scientific Information, Inc.]
日期:2019-03-30
卷期号:25: 2311-2319
被引量:43
摘要
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 AND 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.
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