miR‑34a inhibits esophageal squamous cell carcinoma progression via regulation of FOXM1
Author(s) -
Haibo Zhou,
Yang Li,
Xin-Hua Xu,
Mingqian Lu,
Rong Guo,
Daojun Li,
Qiao Huang,
Yang Liu,
Glenn Deng,
Yalin Xu
Publication year - 2018
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2018.9593
Subject(s) - foxm1 , downregulation and upregulation , oncogene , cancer research , microrna , transfection , cell growth , cell cycle , cell , cell culture , chemistry , cell migration , biology , microbiology and biotechnology , gene , biochemistry , genetics
Downregulation of microRNA-34a (miR-34a) has frequently been observed in esophageal squamous cell carcinoma (ESCC). However, the underlying role and molecular mechanism of miR-34a in ESCC remains largely unknown. In the current study, it was demonstrated that miR-34a was downregulated and forkhead box M1 (FOXM1), a target gene of miR-34a, was upregulated in ESCC tumor tissues. Overexpression of miR-34a decreased FOXM1 mRNA and protein expression in the ESCC cell lines tested (TE-1 and TE-8). Inhibition of miR-34a increased FOXM1 mRNA and protein levels in human esophageal epithelial cells (HEEC). In addition, miR-34a mimics reduced the relative luciferase activity of ESCC cells transfected with FOXM1 3'UTR-WT, but not FOXM1 3'UTR-Mut. The CCK8 assay and scratch wound healing assay showed that overexpression of miR-34a induced inhibition of cell proliferation and cell migration. Additionally, transfection with miR-34a mimics reduced the expression of key genes involved in cell migration (MMP2 and MMP9) in ESCC cells. Thus, the present data demonstrated that miR-34a suppressed ESCC progression by directly targeting FOXM1.
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