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Authors Ma Y, Li X, Chen S, Du B, Li Y
Received 23 August 2018
Accepted for publication 2 December 2018
Published 10 January 2019 Volume 2019:11 Pages 637—649
DOI https://doi.org/10.2147/CMAR.S185117
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 2
Editor who approved publication: Dr Beicheng Sun
Purpose: Increasing
studies have shown that microRNA-4458 (miR-4458) is associated with human
cancer progression. However, the molecular mechanism of miR-4458 in
non-small-cell lung cancer (NSCLC) remains largely unknown. This study aims to
reveal the biological function of miR-4458 in NSCLC.
Materials and methods: The expression
of miR-4458 in NSCLC cells was evaluated by qRT-PCR. Cell proliferation and
migration assay were carried out in vitro after transfection. A luciferase
reporter and Western blot assay were performed to identify the functional
target of miR-4458.
Results: The study
indicated that miR-4458 was markedly downregulated in NSCLC cells.
Overexpression of miR-4458 strongly reduced the proliferation and migration in
NSCLC cell lines. In addition, miR-4458 inhibited the progression of migration
and epithelial–mesenchymal transition (EMT) through the PI3K/AKT pathway.
Luciferase report assay demonstrated that HMGA1 was a target gene for miR-4458.
Conclusion: The results
indicate that miR-4458 participated in the process of migration and EMT via
directly targeting HMGA1 and miR-4458 might be a potential novel therapeutic
target in NSCLC.
Keywords: HMGA1,
migration, epithelial–mesenchymal transition, miR-4458, NSCLC
