Open AccessmiRNA‑199a‑5p suppresses proliferation and invasion by directly targeting NF‑κB1 in human ovarian cancer cells
Author(s) -
Huan Liu,
Baofeng Yao,
Zhiming Wu
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.2018.9170
Subject(s) - lipofectamine , oncogene , microrna , transfection , ovarian cancer , cell growth , cancer research , downregulation and upregulation , cell cycle , cancer cell , biology , chemistry , cancer , cell , cell culture , microbiology and biotechnology , gene , biochemistry , genetics , vector (molecular biology) , recombinant dna
The aberrant expression of microRNA (miRNA)-199a-5p has been frequently reported in a number of cancer types, but to the best of our knowledge, this has not been reported in ovarian cancer (OC). The role and the molecular mechanism of miR-199a-5p in OC have not been reported. Therefore, the present study investigated the effects of miR-199a-5p overexpression on the proliferation and invasion of OC cells. The level of miR-199a-5p in OC cell lines was determined by reverse transcription-quantitative polymerase chain reaction. The miR-199a-5p mimic was transiently transfected into OC cells using Lipofectamine ™ 2000 reagent. Subsequently, the BrdU-ELISA results indicated that the exogenous expression of miR-199a-5p inhibited cell proliferation. In addition, miR-199a-5p overexpression was able to inhibit the invasion of HO-8910 and ES-2 cells. RT-qPCR was performed to determine the expression of matrix metalloproteinase (MMP)-2 and -9 in OC cells. NF-κB1 expression was reduced by upregulation of miR-199a-5p. Bioinformatics analysis predicted that NF-κB1 was a potential target of miR-199a-5p. Luciferase reporter assay further confirmed that miR-199a-5p was able to directly target the 3'UTR of NF-κB1. In conclusion, miRNA-199a-5p may suppress the proliferation and invasion of human ovarian cancer cells by directly targeting NF-κB1.