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30 March 2019 : Laboratory Research  

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

Lizhen Dong1ABCDEF, Guangming Li2ABCDE, Yongmei Li2ABCD, Ze Zhu2ABCDFG*

DOI: 10.12659/MSM.912581

Med Sci Monit 2019; 25:2311-2319


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.

Keywords: PTEN Phosphohydrolase, RNA, Long Noncoding, Down-Regulation, Gene Expression Regulation, Neoplastic, Genes, Tumor Suppressor, Neoplasm Invasiveness, Neoplasm Metastasis, Up-Regulation



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DOI: 10.12659/MSM.939968

Med Sci Monit 2023; 29:e939968


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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750