@Article{096504021X16328213967104,
AUTHOR = {Guojie Chen, Kai Wang, Guoshu Li, Leidong Wang, Yangyang Xiao, Bo Chen},
TITLE = {Long Noncoding RNA LAMTOR5-AS1 Interference Affects MicroRNA-506-3p/ E2F6-Mediated Behavior of Non-Small Cell Lung Cancer Cells},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {9},
PAGES = {945--959},
URL = {http://www.techscience.com/or/v28n9/48487},
ISSN = {1555-3906},
ABSTRACT = {Long noncoding RNA LAMTOR5 antisense RNA 1 (LAMTOR5-AS1) has been certified as a risk predictor and 
diagnostic biomarker of prostate cancer. However, the expression and exact roles of LAMTOR5-AS1 in nonsmall cell lung cancer (NSCLC) remain unclear. Thus, we measured LAMTOR5-AS1 expression in NSCLC 
and gauged its clinical value. The detailed roles and downstream working mechanism of LAMTOR5-AS1 in 
NSCLC were comprehensively unraveled. qRT-PCR was applied to measure gene expression. Functionally, 
utilizing small interfering RNA, LAMTOR5-AS1 was ablated, and the functional alterations were addressed 
by means of different experiments. The targeting activities between LAMTOR5-AS1 and microRNA-506-3p 
(miR-506-3p) and between miR-506-3p and E2F transcription factor 6 (E2F6) were confirmed by RNA immunoprecipitation and luciferase reporter assays. LAMTOR5-AS1 overexpression in NSCLC was verified in 
TCGA datasets and our own cohort and manifested an evident relationship with poor prognosis. Interference 
with LAMTOR5-AS1 led to repression of the proliferation, cloning, and metastasis abilities of NSCLC cells 
in vitro. We further confirmed an obvious increase in LAMTOR5-AS1-silenced NSCLC cell apoptosis. 
Furthermore, the absence of LAMTOR5-AS1 restricted tumor growth in vivo. Mechanistically, LAMTOR5-
AS1 sponged miR-506-3p in NSCLC cells. Furthermore, E2F6, a downstream target of miR-506-3p, was under 
the control of LAMTOR5-AS1, which was realized by decoying miR-506-3p. Rescue experiments showed 
that miR-506-3p suppression or E2F6 reintroduction was capable of remitting LAMTOR5-AS1 deficiencytriggered anticarcinogenic actions in NSCLC. Our study confirmed the exact roles of LAMTOR5-AS1 for the 
first time and revealed that LAMTOR5-AS1 knockdown disrupts the malignancy of NSCLC by targeting the 
miR-506-3p/E2F6 axis. Targeting the LAMTOR5-AS1/miR-506-3p/E2F6 pathway may be instrumental for 
managing patients with NSCLC.},
DOI = {10.3727/096504021X16328213967104}
}