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miR-217-5p suppresses epithelial-mesenchymal transition and the NF-κB signaling pathway in breast cancer via targeting of metadherin.

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机构： [1]Breast Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China. [2]Department of Breast Surgery, Xingtai People's Hospital, Xingtai, Hebei 054000, P.R. China.

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关键词： breast cancer microRNA‑217‑5p epithelial‑mesenchymal transition migration metadherin NF‑κB signaling pathway

摘要：

MicroRNAs (miRNAs) have been associated with a number of human malignancies, including breast cancer (BC). However, the expression, biological function and fundamental underlying mechanism of miR-217-5p in BC remain unclear. Therefore, in the present study, the expression levels of miR-217-5p and metadherin (MTDH) were examined in BC tissues and BC cell lines using reverse transcription-quantitative PCR. Cell Counting Kit-8 assays, cell proliferation, wound healing assays, Transwell assays and western blotting were used to examine the effects of miR-217-5p on cell proliferation, migration, the epithelial-mesenchymal transition (EMT) and NF-κB signaling pathway expression. The direct relationship between miR-217-5p and MTDH was assessed using a dual-luciferase reporter assay. The results demonstrated that significantly reduced expression levels of miR-217-5p but significantly increased mRNA expression levels of MTDH were observed in BC tissues from 35 patients with BC compared with non-tumor breast tissues. Furthermore, BC cell lines SK-BR3 and BT549 expressed miR-217-5p at markedly lower levels and MTDH at markedly higher levels compared with the breast epithelial MCF10A cell line. miR-217-5p overexpression significantly inhibited cell proliferation, invasion and migration and suppressed the EMT in BC cells. miR-217-5p overexpression also inhibited the NF-κB signaling pathway by markedly decreasing p65 mRNA and protein expression levels but significantly increasing IκBα expression levels. Furthermore, miR-217-5p knockdown markedly increased MTDH mRNA and protein expression levels. The expression levels of miR-217-5p were negatively correlated with those of MTDH in BC tissues. These results suggested that restoration of MTDH expression levels could potentially attenuate the inhibitory effects of miR-217-5p overexpression on BC cell proliferation. Therefore, in conclusion miR-217-5p overexpression may inhibit cell migration, invasion, the EMT and NF-κB signaling pathway in BC via targeting of MTDH. miR-217-5p may serve as an important potential target in BC therapy.Copyright: © Yang et al.

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出版当年[2022]版：

大类 | 4 区医学

小类 | 4 区肿瘤学

最新[2025]版：

大类 | 4 区医学

小类 | 4 区肿瘤学

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Q3 ONCOLOGY

最新[2023]版：

Q3 ONCOLOGY

影响因子： 2.5 最新[2023版] 2.4 最新五年平均 2.9 出版当年[2022版] 2.6 出版当年五年平均 3.111 出版前一年[2021版] 2.5 出版后一年[2023版]

第一作者：

第一作者机构： [1]Breast Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China. [2]Department of Breast Surgery, Xingtai People's Hospital, Xingtai, Hebei 054000, P.R. China.

通讯作者：

通讯机构： [1]Breast Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China. [*1]Breast Center, The Fourth Hospital of Hebei Medical University, 169 Changjiang Avenue, Shijiazhuang, Hebei 050000, P.R. China

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miR-217-5p suppresses epithelial-mesenchymal transition and the NF-κB signaling pathway in breast cancer via targeting of metadherin.

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