MicroRNA-211 promotes non-small-cell lung cancer proliferation and invasion by targeting MxA

Mafei Kang, Jieqiong Shi, Na Peng, Shaozhong He Department of Medical Oncology, Affiliated Hospital of Guilin Medical College, Guilin, People’s Republic of China Abstract: Recent studies have shown that microRNAs play a pivotal role in the pathogenesis of cancer. In our current study, th...

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Bibliographic Details
Main Authors: Kang M, Shi J, Peng N, He S
Format: Article
Language:English
Published: Dove Medical Press 2017-11-01
Series:OncoTargets and Therapy
Subjects:
MxA
Online Access:https://www.dovepress.com/microrna-211-promotes-non-small-cell-lung-cancer-proliferation-and-inv-peer-reviewed-article-OTT
Description
Summary:Mafei Kang, Jieqiong Shi, Na Peng, Shaozhong He Department of Medical Oncology, Affiliated Hospital of Guilin Medical College, Guilin, People’s Republic of China Abstract: Recent studies have shown that microRNAs play a pivotal role in the pathogenesis of cancer. In our current study, the expression levels of microRNA-211 (miR-211) were measured in human non-small-cell lung cancer (NSCLC) tissues and cell lines. We found that miR-211 expression levels were increased in NSCLC tissues and cell lines and that the overexpression of miR-211 promotes cell proliferation and invasion. Using bioinformatics, we demonstrated that miR-211 binds to the 3'-untranslated region of MxA and overexpression of miR-211 suppresses the expression of MxA at both the transcriptional and translational levels in NSCLC cell lines. Furthermore, knockdown of MxA increased the proliferation and invasion of NSCLC cell lines in vitro. High levels of miR-211 expression were associated with a shorter survival time in patients with NSCLC. Taken together, these results suggest that miR-211 promotes tumor proliferation and invasion by regulating MxA expression in NSCLC. This study provides insights into molecular mechanisms of miR-211-mediated tumorigenesis and oncogenesis. Keywords: miR-211, MxA, non-small-cell lung cancer, proliferation, invasion
ISSN:1178-6930