@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} }