Open Access

Inhibition of miR‑214 attenuates the migration and invasion of triple‑negative breast cancer cells

  • Authors:
    • Yi Zhang
    • Zhijing Zhao
    • Siqi Li
    • Liying Dong
    • Yan Li
    • Ying Mao
    • Ying Liang
    • Yun Tao
    • Junfeng Ma
  • View Affiliations

  • Published online on: April 1, 2019     https://doi.org/10.3892/mmr.2019.10112
  • Pages: 4035-4042
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Triple‑negative breast cancer (TNBC) is a subtype of breast cancer. MicroRNA (miR)‑214 is closely associated with controlling the development of tumor cells; therefore, in the present study, the target gene and effects of miR‑214 on TNBC cells were explored. Luciferase activity was examined by luciferase reporter assay. The viability, invasion and migration of MDA‑MB‑231 TNBC cells were measured using Cell Counting kit‑8, Transwell and wound‑healing assays, respectively. The expression levels of various factors were determined using reverse transcription‑quantitative polymerase chain reaction and western blotting. The results demonstrated that the expression levels of miR‑214 were higher and the levels of α1‑antitrypsin (α1‑AT) were lower in TNBC tissues compared with in normal tissues. Subsequently, α1‑AT was revealed to be a target of miR‑214. Furthermore, inhibition of miR‑214 decreased cell viability, invasion and migration, enhanced the expression of E‑cadherin and tissue inhibitor of metalloproteinases‑2, and reduced the expression of metastatic tumour antigen 1 and matrix metalloproteinase‑2. Inhibition of miR‑214 also significantly downregulated the phosphorylation of protein kinase B (Akt) and mammalian target of rapamycin (mTOR), and markedly downregulated that of phosphoinositide 3‑kinase (PI3K); however, the expression levels of total PI3K, Akt and mTOR remained stable in all groups. Taken together, these findings indicated that α1‑AT may be a target of miR‑214. Downregulation of miR‑214 markedly suppressed the viability, migration and invasion of MDA‑MB‑231 cells, and inhibited the PI3K/Akt/mTOR pathway. These findings suggested that miR‑214 targeting α1‑AT may be a potential mechanism underlying TNBC development.
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May-2019
Volume 19 Issue 5

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Zhang Y, Zhao Z, Li S, Dong L, Li Y, Mao Y, Liang Y, Tao Y and Ma J: Inhibition of miR‑214 attenuates the migration and invasion of triple‑negative breast cancer cells. Mol Med Rep 19: 4035-4042, 2019.
APA
Zhang, Y., Zhao, Z., Li, S., Dong, L., Li, Y., Mao, Y. ... Ma, J. (2019). Inhibition of miR‑214 attenuates the migration and invasion of triple‑negative breast cancer cells. Molecular Medicine Reports, 19, 4035-4042. https://doi.org/10.3892/mmr.2019.10112
MLA
Zhang, Y., Zhao, Z., Li, S., Dong, L., Li, Y., Mao, Y., Liang, Y., Tao, Y., Ma, J."Inhibition of miR‑214 attenuates the migration and invasion of triple‑negative breast cancer cells". Molecular Medicine Reports 19.5 (2019): 4035-4042.
Chicago
Zhang, Y., Zhao, Z., Li, S., Dong, L., Li, Y., Mao, Y., Liang, Y., Tao, Y., Ma, J."Inhibition of miR‑214 attenuates the migration and invasion of triple‑negative breast cancer cells". Molecular Medicine Reports 19, no. 5 (2019): 4035-4042. https://doi.org/10.3892/mmr.2019.10112