@Article{096504019X15732109856009,
AUTHOR = {ZiJun Liao, Qi Zheng, Ting Wei, YanBing Zhang, JieQun Ma, Zheng Zhao, 
HaiFeng Sun, KeJun Nan},
TITLE = {MicroRNA-561 Affects Proliferation and Cell Cycle Transition Through  PTEN/AKT Signaling Pathway by Targeting P-REX2a in NSCLC},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {2},
PAGES = {147--159},
URL = {http://www.techscience.com/or/v28n2/48540},
ISSN = {1555-3906},
ABSTRACT = {MicroRNAs (miRNAs) play crucial roles in tumorigenesis and tumor progression. miR-561 has been reported 
to be downregulated in gastric cancer and affects cancer cell proliferation and metastasis. However, the role and 
underlying molecular mechanism of miR-561 in human non-small cell lung cancer (NSCLC) remain unknown 
and need to be further elucidated. In this study, we discovered that miR-561 expression was downregulated 
in human NSCLC tissues and cell lines. The overexpression of miR-561 inhibited NSCLC cell proliferation 
and cell cycle G1
/S transition and induced apoptosis. The inhibition of miR-561 facilitated cell proliferation 
and G1
/S transition and suppressed apoptosis. miR-561 expression was inversely correlated with P-REX2a 
expression in NSCLC tissues. P-REX2a was confirmed to be a direct target of miR-561 using a luciferase 
reporter assay. The overexpression of miR-561 decreased P-REX2a expression, and the suppression of miR-
561 increased P-REX2a expression. Particularly, P-REX2a silencing recapitulated the cellular and molecular effects observed upon miR-561 overexpression, and P-REX2a overexpression counteracted the effects of 
miR-561 overexpression on NSCLC cells. Moreover, both exogenous expression of miR-561 and silencing of 
P-REX2a resulted in suppression of the PTEN/AKT signaling pathway. Our study demonstrates that miR-561 
inhibits NSCLC cell proliferation and G1
/S transition and induces apoptosis through suppression of the PTEN/
AKT signaling pathway by targeting P-REX2a. These findings indicate that miR-561 plays a significant role in 
NSCLC progression and serves as a potential therapeutic target for NSCLC.},
DOI = {10.3727/096504019X15732109856009}
}