科研之友
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摘要
The purpose of the present study was to investigate the effects of upregulating microRNA (miR)-181b expression in tumor-associated macrophages regarding breast cancer cell metastasis and to identify the target gene. Ectopic miR-181b was transfected into MDA-MB-231 and MCF-7 breast cancer cell lines with or without chemokine ligand 18 (CCL18) stimulation. Cell proliferation, migration/invasion and apoptosis rate were investigated. The binding effects of miR-181b to the 3'-untranslated region (UTR) of the nuclear factor (NF)-kappa B gene were detected with the dual luciferase reporter system. Immunofluorescent staining of the NF-kappa B key component P65 was performed. The messenger (m) RNA and protein expression of NF-kappa B induced by CCL18 with or without miR-181b stimulation was evaluated with reverse transcription -quantitative polymerase chain reaction and western blot analysis. When compared with the CCL18-stimulated group, miR-181b mimic-transfected cells exhibited significantly inhibited proliferation. and migration, with an increased cell apoptosis percentage in a dose-dependent manner. Furthermore, the luciferase activity was reduced for cells with NF-kappa B 3'-UTR wild-type that were co-transfected with miR-181b mimics. Immunofluorescent staining of NF-kappa B demonstrably weakened the P65 signal in stimulated miR-181b mimic cells when compared with parental and CCL18-treated cells. The increased expression level of NF-kappa B induced by CCL18 in MDA-MB-231 and MCF-7 cells was suppressed by miR-181b mimics. Overexpression of miR-181b suppressed cell survival rate and migration. This overexpression may achieve this goal by regulating the NF-kappa B pathway in breast cancer cells. Our study demonstrated a potential therapeutic application of miR-181b in the treatment of breast cancer.
- 出版日期2016-12
- 单位新乡医学院
