Hsa-miR-625 Upregulation Promotes Apoptosis in Acute Myeloid Leukemia Cell Line by Targeting Integrin-linked Kinase Pathway

Document Type : Research Articles


1 Department of Hematology, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran.

2 Department of Regenerative Biomedicine, Cell Science Research Center, Royan Institute for Stem Cell Biology & Technology, ACECR, Tehran, Iran.

3 Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology & Technology, ACECR, Tehran, Iran.


Background: Growing evidence has demonstrated that microRNAs have a major effect on development of different types of cancer including AML. The overexpression of miR-625 could decrease tumorgenesis of acute myeloid leukemia cell lines through Integrin-linked kinase signaling pathway and reducing the associated oncogenes.  The aim of this study is to evaluate the effect of hsa-miR-625 upregulation on apoptosis and proliferation of KG1 cell line via ILK signaling pathway. Methods: The KG-1 cell line was transfected with pLenti-III-premir625-GFP through viral method. Then, expression of miR-625 and genes were analyzed by quantitative PCR. Western blotting was used to evaluate for the protein level. Apoptosis was investigated by flow cytometry. Cell cycle analysis with PI and CCK-8 assay were performed to evaluate proliferation. Results: KG-1 cells transfected with pLenti-III-pre mir625-GFP construct showed a significant increase in cell apoptosis. Gene expression of ILK and NF-κB were downregulated and AKT, c-fos, Caspase3, cyclin D1, KLF-4, OCT-4 and Nanog were upregulated but no alteration in GSK3 expression profile was observed. Downregulation of NF-κB and upregulation of Caspase 3 and p-β-catenin protein levels were indicated (p<0.05). Conclusion: MiR-625 can be a promising approach to aid in the treatment of AML. However, further studies are required in this respect.


Main Subjects

Volume 23, Issue 4
April 2022
Pages 1159-1167
  • Receive Date: 28 December 2020
  • Revise Date: 31 May 2021
  • Accept Date: 21 April 2022
  • First Publish Date: 21 April 2022