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Authors Wang L, Wang Y, Du X, Yao Y, Wang L, Jia Y
Received 22 January 2019
Accepted for publication 26 February 2019
Published 18 April 2019 Volume 2019:12 Pages 2999—3009
DOI https://doi.org/10.2147/OTT.S202523
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Ms Shreya Arora
Peer reviewer comments 2
Editor who approved publication: Dr William Cho
Background/aims: MiR-216b
and forkhead box M1 (FOXM1) were demonstrated to exert their biological effects
on the development and progression of tumors. This study aimed to investigate
the expression and role of miR-216b and FOXM1 in tissues and cell lines of
non-small cell lung cancer (NSCLC).
Methods: The
expressions of miR-216b and FOXM1 in NSCLC tissues and cells were detected by
qRT-PCR and Western blot analysis. Cell proliferation was measured by CCK-8
assay. Cell migration and invasion were confirmed by Transwell assay. Finally,
the bioinformatics and dual-luciferase reporter assay were conducted to
validate the relationship of miR-216b and FOXM1.
Results: Compared
with normal tissues and cells, the expression of miR-216b was obviously
decreased in NSCLC tissues and cells. However, the expressions of FOXM1 mRNA
and protein were significantly increased, and negatively correlated with the
expression of miR-216b. Multivariate Cox’s regression analysis suggested that
miR-216b or FOXM1 expression was an independent prognostic factor for patients
with NSCLC. MiR-216b overexpression remarkably repressed cell proliferation,
migration, invasion, and epithelial–mesenchymal transition (EMT) of NSCLC
cells. The bioinformatics and dual-luciferase reporter assay validated that the
3ʹ-untranslated region (3ʹ-UTR) of FOXM1 mRNA was indeed a direct target of
FOXM1. In vitro, overexpression of FOXM1 partially eliminated inhibitory
effects of miR-216b on cell proliferation, migration, and invasion, whereas
inhibition of FOXM1 contributed to inhibitory effects mediated by miR-216b.
Conclusion: MiR-216b
inhibits cell proliferation, migration, invasion, and EMT by targeting the
expression of FOXM1 in human NSCLC. These findings suggested a potential therapeutic
role of miR-216b in patients of NSCLC.
Keywords: MiR-216b,
FOXM1, NSCLC, suppressor