@Article{096504017X14973124850905,
AUTHOR = {Dandan Li, Changjun He, Junfeng Wang, Yanbo Wang, Jianlong Bu, Xianglong Kong, Dawei Sun},
TITLE = {MicroRNA-138 Inhibits Cell Growth, Invasion, and EMT of Non-Small Cell  Lung Cancer via SOX4/p53 Feedback Loop},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {3},
PAGES = {385--400},
URL = {http://www.techscience.com/or/v26n3/56651},
ISSN = {1555-3906},
ABSTRACT = {Many studies have shown that downregulation of miR-138 occurs in a variety of cancers including non-small 
cell lung cancer (NSCLC). However, the precise mechanisms of miR-138 in NSCLC have not been well clarified. In this study, we investigated the biological functions and molecular mechanisms of miR-138 in NSCLC 
cell lines, discussing whether it could turn out to be a therapeutic biomarker of NSCLC in the future. In our 
study, we found that miR-138 is downregulated in NSCLC tissues and cell lines. Moreover, the low level of 
miR-138 was associated with increased expression of SOX4 in NSCLC tissues and cell lines. Upregulation 
of miR-138 significantly inhibited proliferation of NSCLC cells. In addition, invasion and EMT of NSCLC 
cells were suppressed by overexpression of miR-138. However, downregulation of miR-138 promoted cell 
growth and metastasis of NSCLC cells. Bioinformatics analysis predicted that SOX4 was a potential target gene of miR-138. Next, luciferase reporter assay confirmed that miR-138 could directly target SOX4. 
Consistent with the effect of miR-138, downregulation of SOX4 by siRNA inhibited proliferation, invasion, 
and EMT of NSCLC cells. Overexpression of SOX4 in NSCLC cells partially reversed the effect of miR-138 
mimic. In addition, decreased SOX4 expression could increase the level of miR-138 via upregulation of p53. 
Introduction of miR-138 dramatically inhibited growth, invasion, and EMT of NSCLC cells through a SOX4/
p53 feedback loop.},
DOI = {10.3727/096504017X14973124850905}
}