Open Access

MicroRNA‑93 knockdown inhibits acute myeloid leukemia cell growth via inactivating the PI3K/AKT pathway by upregulating DAB2

  • Authors:
    • Jiwei Huang
    • Ruozhi Xiao
    • Xiaozhen Wang
    • Bijay Khadka
    • Zhigang Fang
    • Mingxue Yu
    • Ling Zhang
    • Jieying Wu
    • Jiajun Liu
  • View Affiliations

  • Published online on: September 2, 2021     https://doi.org/10.3892/ijo.2021.5260
  • Article Number: 81
  • Copyright: © Huang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Acute myeloid leukemia (AML) is associated with a poor prognosis in elderly adults and currently lacks optimal treatment strategies. MicroRNAs (miRNAs or miRs) have increasingly been reported to be associated with AML progression; however, the mechanisms of action of miR‑93 in AML with the involvement of disabled 2 (DAB2) are currently unknown. In the present study, miR‑93 expression was assessed in patients with AML and in AML cell lines. The association between miR‑93 expression and the pathological characteristics of patients with AML was analyzed. AML cells were then transfected to knockdown or overexpress miR‑93 in order to elucidate its function in AML progression. The target gene of miR‑93 was assessed using a dual‑luciferase reporter gene assay. The expression levels of miR‑93, DAB2 and phosphatidylinositol 3‑kinase (PI3K)/protein kinase B (AKT) pathway‑related proteins were measured and in vivo experiments were conducted to confirm the results. It was observed that miR‑93 was highly expressed in patients with AML and in AML cells. The knockdown of miR‑93 in HL‑60 cells inhibited AML cell proliferation and resistance to apoptosis, while the overexpression of miR‑93 in THP‑1 cells led to contrasting results. Moreover, miR‑93 targeted DAB2 to inactivate the PI3K/AKT pathway, and the overexpression of DAB2 reversed the effects of miR‑93 on THP‑1 cell growth. Tumor volume, tumor weight, and the positive expression of Ki67, survivin and p53 were increased in THP‑1 cells overexpressing miR‑93. On the whole, the present study demonstrates that miR‑93 is highly expressed in AML cells, and that the suppression of miR‑93 inhibits AML cell growth by targeting DAB2 and inhibiting the PI3K/AKT pathway.
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October-2021
Volume 59 Issue 4

Print ISSN: 1019-6439
Online ISSN:1791-2423

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Spandidos Publications style
Huang J, Xiao R, Wang X, Khadka B, Fang Z, Yu M, Zhang L, Wu J and Liu J: MicroRNA‑93 knockdown inhibits acute myeloid leukemia cell growth via inactivating the PI3K/AKT pathway by upregulating DAB2. Int J Oncol 59: 81, 2021
APA
Huang, J., Xiao, R., Wang, X., Khadka, B., Fang, Z., Yu, M. ... Liu, J. (2021). MicroRNA‑93 knockdown inhibits acute myeloid leukemia cell growth via inactivating the PI3K/AKT pathway by upregulating DAB2. International Journal of Oncology, 59, 81. https://doi.org/10.3892/ijo.2021.5260
MLA
Huang, J., Xiao, R., Wang, X., Khadka, B., Fang, Z., Yu, M., Zhang, L., Wu, J., Liu, J."MicroRNA‑93 knockdown inhibits acute myeloid leukemia cell growth via inactivating the PI3K/AKT pathway by upregulating DAB2". International Journal of Oncology 59.4 (2021): 81.
Chicago
Huang, J., Xiao, R., Wang, X., Khadka, B., Fang, Z., Yu, M., Zhang, L., Wu, J., Liu, J."MicroRNA‑93 knockdown inhibits acute myeloid leukemia cell growth via inactivating the PI3K/AKT pathway by upregulating DAB2". International Journal of Oncology 59, no. 4 (2021): 81. https://doi.org/10.3892/ijo.2021.5260