Open Access
ARTICLE
Long Noncoding RNA LAMTOR5-AS1 Interference Affects MicroRNA-506-3p/ E2F6-Mediated Behavior of Non-Small Cell Lung Cancer Cells
Guojie Chen*1, Kai Wang*1, Guoshu Li†1, Leidong Wang‡, Yangyang Xiao§, Bo Chen¶
* Department of Oncology, The First People’s Hospital of Yancheng, The Fourth Affiliated Hospital of Nantong University,
Jiangsu, P. R. China
† Department of Respiratory Medicine, Shanghai Tenth People’s Hospital, Tongji University School of Medicine,
Shanghai, P. R. China
‡ Department of Pathology, Binzhou Medical University Hospital, Shandong, P. R. China
§ Department of Clinical Laboratory, Binzhou Medical University Hospital, Shandong, P. R. China
¶ Department of Infectious Disease, The First People’s Hospital of Yancheng, The Fourth Affiliated Hospital of Nantong University,
Jiangsu, P. R. China
Oncology Research 2020, 28(9), 945-959. https://doi.org/10.3727/096504021X16328213967104
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.
Keywords
Cite This Article
APA Style
Chen, G., Wang, K., Li, G., Wang, L., Xiao, Y. et al. (2020). Long noncoding RNA LAMTOR5-AS1 interference affects microrna-506-3p/ e2f6-mediated behavior of non-small cell lung cancer cells. Oncology Research, 28(9), 945-959. https://doi.org/10.3727/096504021X16328213967104
Vancouver Style
Chen G, Wang K, Li G, Wang L, Xiao Y, Chen B. Long noncoding RNA LAMTOR5-AS1 interference affects microrna-506-3p/ e2f6-mediated behavior of non-small cell lung cancer cells. Oncol Res. 2020;28(9):945-959 https://doi.org/10.3727/096504021X16328213967104
IEEE Style
G. Chen, K. Wang, G. Li, L. Wang, Y. Xiao, and B. Chen "Long Noncoding RNA LAMTOR5-AS1 Interference Affects MicroRNA-506-3p/ E2F6-Mediated Behavior of Non-Small Cell Lung Cancer Cells," Oncol. Res., vol. 28, no. 9, pp. 945-959. 2020. https://doi.org/10.3727/096504021X16328213967104