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Article Open Access

miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2

  • Authors:
    • Xiaohe Chen
    • Shouhang Yang
    • Jue Zeng
    • Ming Chen
  • View Affiliations / Copyright

    Affiliations: Department of Blood Transfusion, The Third Affiliated Hospital of Wenzhou Medical University, Ruian, Zhejiang 325200, P.R. China
    Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 508-514
    |
    Published online on: November 21, 2018
       https://doi.org/10.3892/mmr.2018.9680
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Abstract

MicroRNAs (miRNAs) have been demonstrated to regulate the progression of numerous types of cancer, including acute myeloid leukemia (AML). Previous studies demonstrated that miR‑1271‑5p functions as a tumor suppressor; however, the roles of miR‑1271‑5p in AML remain unknown. In the present study, miR‑1271‑5p was significantly downregulated in AML tissues compared with normal tissues by reverse transcription‑quantitative polymerase chain reaction analysis. Furthermore, the expression levels of miR‑1271‑5p in patients with AML may function as a prognostic marker. In addition, overexpression of miR‑1271‑5p significantly suppressed the proliferation and induced apoptosis of AML cells by Cell Counting kit‑8 and fluorescence activated cell sorter assays; miR‑1271‑5p downregulation exhibited opposing effects. Additionally, transcription factor ZIC2 may be a direct target of miR‑1271‑5p in AML cells, which was demonstrated by a luciferase reporter assay and RNA pulldown assay. Overexpression of miR‑1271‑5p significantly reduced the mRNA and protein expression levels of ZIC2 in AML193 and OCI‑AML2 cells by reverse transcription‑quantitative polymerase chain reaction analysis and western blotting. Furthermore, an inverse correlation between miR‑1271‑5p and ZIC2 expression in AML samples was observed. In summary, ZIC2 was upregulated in AML tissues, and restoration of ZIC2 expression was able to promote the proliferation and reduce the apoptosis of AML cells transfected with miR‑1271‑5p mimics. The results of the present study demonstrated that miR‑1271‑5p inhibited the progression of AML by targeting ZIC2.
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Copy and paste a formatted citation
Spandidos Publications style
Chen X, Yang S, Zeng J and Chen M: miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2. Mol Med Rep 19: 508-514, 2019.
APA
Chen, X., Yang, S., Zeng, J., & Chen, M. (2019). miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2. Molecular Medicine Reports, 19, 508-514. https://doi.org/10.3892/mmr.2018.9680
MLA
Chen, X., Yang, S., Zeng, J., Chen, M."miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2". Molecular Medicine Reports 19.1 (2019): 508-514.
Chicago
Chen, X., Yang, S., Zeng, J., Chen, M."miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2". Molecular Medicine Reports 19, no. 1 (2019): 508-514. https://doi.org/10.3892/mmr.2018.9680
Copy and paste a formatted citation
x
Spandidos Publications style
Chen X, Yang S, Zeng J and Chen M: miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2. Mol Med Rep 19: 508-514, 2019.
APA
Chen, X., Yang, S., Zeng, J., & Chen, M. (2019). miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2. Molecular Medicine Reports, 19, 508-514. https://doi.org/10.3892/mmr.2018.9680
MLA
Chen, X., Yang, S., Zeng, J., Chen, M."miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2". Molecular Medicine Reports 19.1 (2019): 508-514.
Chicago
Chen, X., Yang, S., Zeng, J., Chen, M."miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2". Molecular Medicine Reports 19, no. 1 (2019): 508-514. https://doi.org/10.3892/mmr.2018.9680
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