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

  • Authors:
    • Lixian Yang
    • Shuo Liu
    • Liu Yang
    • Bin Xu
    • Meiqi Wang
    • Xiangshun Kong
    • Zhenchuan Song

  • View Affiliations

  • Published online on: March 23, 2022     https://doi.org/10.3892/ol.2022.13282
  • Article Number: 162

  • Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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.
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May-2022
Volume 23 Issue 5

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Yang L, Liu S, Yang L, Xu B, Wang M, Kong X and Song Z: miR‑217‑5p suppresses epithelial‑mesenchymal transition and the NF‑κB signaling pathway in breast cancer via targeting of metadherin. Oncol Lett 23: 162, 2022
APA
Yang, L., Liu, S., Yang, L., Xu, B., Wang, M., Kong, X., & Song, Z. (2022). miR‑217‑5p suppresses epithelial‑mesenchymal transition and the NF‑κB signaling pathway in breast cancer via targeting of metadherin. Oncology Letters, 23, 162. https://doi.org/10.3892/ol.2022.13282
MLA
Yang, L., Liu, S., Yang, L., Xu, B., Wang, M., Kong, X., Song, Z."miR‑217‑5p suppresses epithelial‑mesenchymal transition and the NF‑κB signaling pathway in breast cancer via targeting of metadherin". Oncology Letters 23.5 (2022): 162.
Chicago
Yang, L., Liu, S., Yang, L., Xu, B., Wang, M., Kong, X., Song, Z."miR‑217‑5p suppresses epithelial‑mesenchymal transition and the NF‑κB signaling pathway in breast cancer via targeting of metadherin". Oncology Letters 23, no. 5 (2022): 162. https://doi.org/10.3892/ol.2022.13282