Open AccessmiR‑425‑5p promotes cell proliferation, migration and invasion by directly targeting FOXD3 in hepatocellular carcinoma cells
Author(s) -
Haijian Wu,
Jia Shang,
Weili Zhan,
Junping Liu,
Huibin Ning,
Ning Chen
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10427
Subject(s) - oncogene , cell growth , cancer research , gene knockdown , carcinogenesis , cell cycle , microrna , downregulation and upregulation , epithelial–mesenchymal transition , cell , biology , cell migration , apoptosis , metastasis , hepatocellular carcinoma , cancer , gene , biochemistry , genetics
MicroRNAs (miRs) are important regulators of the tumorigenesis and metastasis of various cancers. In the present study, the roles and underlying mechanisms of miR‑425‑5p in the development of hepatocellular carcinoma (HCC) were investigated. RT‑qPCR analysis revealed that miR‑425‑5p was upregulated in HCC tissues and cell lines. A functional study in vitro using MTT assays, colony formation and Transwell assays demonstrated that overexpression of miR‑425‑5p promoted the proliferation, migration, and invasion of HCC cells, prevented cell apoptosis and accelerates the epithelial‑mesenchymal transition process, whereas miR‑425‑5p knockdown induced opposing effects. A further mechanistic study revealed that forkhead box D3 (FOXD3) was a direct target of miR‑425‑5p, and gain‑ and loss‑of‑function of FOXD3 studies demonstrated that FOXD3 suppressed HCC cell proliferation, migration, and invasion. Furthermore, rescue experiments revealed that overexpression of FOXD3 counteracted the positive effects of miR‑425‑5p on HCC malignant behaviors. Collectively, the present results demonstrated that miR‑425‑5p promoted HCC cell proliferation, migration, and invasion by suppressing FOXD3 expression, potentially providing a novel target for the treatment of HCC.