@Article{096504016X14570992647168,
AUTHOR = {Yuefeng Ma, Jie Feng, Xin Xing, Bin Zhou, Shaomin Li, Wei Zhang, Jiantao Jiang, Jin Zhang, Zhe Qiao, Liangzhang Sun, Zhenchuan Ma, Ranran Kong},
TITLE = {miR-1908 Overexpression Inhibits Proliferation, Changing Akt Activity and p53 Expression in Hypoxic NSCLC Cells},
JOURNAL = {Oncology Research},
VOLUME = {24},
YEAR = {2016},
NUMBER = {1},
PAGES = {9--15},
URL = {http://www.techscience.com/or/v24n1/56605},
ISSN = {1555-3906},
ABSTRACT = {The ribosomal protein (RP)–p53 pathway has been shown to play a key role in apoptosis and senescence 
of cancer cells. miR-1908 is a newly found miRNA that was reported to have prognostic potential in melanoma. However, its role and mechanism in the progression of non-small cell lung cancer (NSCLC) are largely 
unknown. In this study, we found that expression of miR-1908 was significantly downregulated in human 
NSCLC cell lines, including SK-MES-1, A549, and NCI-H460. Then the role of miR-1908 in NSCLC cell 
proliferation was explored. The miR-1908 mimic was transfected into NSCLC cell lines, and their proliferation was detected. MTT and Cell Titer-Blue H analyses showed that the cell proliferation was notably reduced 
by the miR-1908 mimic transfection. Moreover, we found the RP–p53 pathway was activated by miR-1908 
mimic. Moreover, the miR-1908 inhibitor transfection had a completely opposite effect on the NSCLC cell 
proliferation than that of miR-1908 mimic. To explore the underlying mechanism of that, TargetScan bioinformatics server and 3'-UTR luciferase reporter assay were applied to identify the targets of miR-1908. Our results 
showed that AKT1 substrate 1 (AKT1S1), a newly proven suppressor of the RP–p53 pathway, was a target of 
miR-1908, suggesting a probable mechanism for miR-191 suppressing NSCLC cell proliferation. Our findings 
provide a novel molecular target for the regulation of NSCLC cell proliferation.},
DOI = {10.3727/096504016X14570992647168}
}