@Article{096504017X14850182723737,
AUTHOR = {Yingbo Xue, Tingting Ni, Ying Jiang, Yong Li},
TITLE = {Long Noncoding RNA GAS5 Inhibits Tumorigenesis and Enhances  Radiosensitivity by Suppressing miR-135b Expression  in Non-Small Cell Lung Cancer},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {8},
PAGES = {1305--1316},
URL = {http://www.techscience.com/or/v25n8/56915},
ISSN = {1555-3906},
ABSTRACT = {Growth arrest-specific transcript 5 (GAS5) has been demonstrated to correlate with clinicopathological characteristics and serve as a tumor suppressor in non-small cell lung cancer (NSCLC). However, the underlying mechanism of the competing endogenous RNA (ceRNA) regulatory network involving GAS5 in NSCLC 
remains to be elucidated. In this study, qRT-PCR results showed that GAS5 was downregulated and miR-135b 
was upregulated in NSCLC tissues and cells. The expressions of GAS5 and miR-135b changed inversely 
in response to irradiation. Gain-of-function experiments revealed that GAS5 overexpression and miR-135b 
downregulation significantly suppressed tumorigenesis by repressing cell proliferation and invasion, and 
enhanced the radiosensitivity of NSCLC cells by reducing colony formation rates. Luciferase reporter assay 
confirmed that GAS5 could directly target miR-135b and negatively regulate its expression. Moreover, rescue experiments demonstrated that miR-135b upregulation markedly abolished GAS5 overexpression-induced 
tumorigenesis inhibition and radiosensitivity improvement. Furthermore, xenograft model analysis validated 
that GAS5 overexpression suppressed tumor growth and improved radiosensitivity of NSCLC cells in vivo. 
Taken together, GAS5 inhibits tumorigenesis and enhances radiosensitivity by suppressing miR-135b expression in NSCLC cells, deepening our understanding of the mechanism of miRNA–lncRNA interaction and 
providing a novel therapeutic strategy for NSCLC.},
DOI = {10.3727/096504017X14850182723737}
}