@Article{096504016X14822800040451,
AUTHOR = {Yongcheng Mei, Jinchun Si, Yun Wang, Zhuangshi Huang, Haiwen Zhu, Shijun Feng, Xuezhi Wu, Liwen Wu},
TITLE = {Long Noncoding RNA GAS5 Suppresses Tumorigenesis by Inhibiting  miR-23a Expression in Non-Small Cell Lung Cancer},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {6},
PAGES = {1027--1037},
URL = {http://www.techscience.com/or/v25n6/56885},
ISSN = {1555-3906},
ABSTRACT = {Previous studies reported that elevated expression of long noncoding RNA (lncRNA) GAS5 led to the arrest 
of non-small cell lung cancer (NSCLC) cell growth and a promotion of apoptosis both in vitro and in vivo. 
However, its underlying molecular mechanism in NSCLC is still unclear. In the present study, we noted that 
GAS5 was downregulated in NSCLC tissues and cells and was negatively correlated with miR-23a expression. 
Luciferase reporter assay and qRT-PCR analysis demonstrated that GAS5 directly interacted with miR-23a 
and reversely regulated its expression. miR-23a overexpression markedly promoted NSCLC cell proliferation and invasion, while GAS5 overexpression dramatically inhibited NSCLC cell proliferation and invasion 
and promoted apoptosis. Functional analysis indicated that miR-23a overexpression significantly abolished 
GAS5 overexpression-induced inhibition of proliferation and invasion, as well as promotion of apoptosis in 
NSCLC cells. Moreover, xenograft experiments further revealed that upregulation of GAS5 notably impaired 
the growth of transplanted tumors by suppressing miR-23a in nude mice. These results suggested that overexpression of lncRNA GAS5 inhibits tumorigenesis of NSCLC by inhibiting miR-23a in vitro and in vivo, 
providing a potential therapeutic strategy for patients with NSCLC.},
DOI = {10.3727/096504016X14822800040451}
}