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Bioimpacts. 2017;7(2): 109-114.
doi: 10.15171/bi.2017.14
PMID: 28752075
PMCID: PMC5524985
Scopus ID: 85027458202
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Original Research

miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1

Mahdi Edalati Fathabad 1, Morteza Karimipoor 2*, Shaban Alizadeh 1*, Asghar Abdoli 3, Amir Atashi 4, Mahtab Sayadi 4

1 Hematology Department, School of Allied Medicine, Tehran University of Medical Sciences, Tehran, Iran
2 Molecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran
3 Department of Hepatitis and AIDS, Pasteur Institute of Iran, Tehran, Iran
4 Cancer Prevention Research Center, Shahroud University of Medical Sciences, Shahroud, Iran
*Corresponding Authors: Email: mortezakarimi@pasteur.ac.ir; Email: alizadeh1982@gmail.com

Abstract

Introduction: Chronic myelogenous leukemia (CML) is a myeloproliferative disorder caused by the Philadelphia chromosome translocation, at (9; 22), which results in BCR-ABL fusion tyrosine kinase oncoprotein. This fusion induces down-regulation of miR-155. Upregulation of miR-155 can influence cell fate via the effect on p27kip1 and apoptosis. The aim of this study was to induce apoptosis in K562 CML cell line by overexpression of miR-155.
Methods:
The K562 cell line was transfected with pLenti-III-pre mir155-GFP constructs through electroporation. Then, overexpression of miR-155 as well as the expression level of p27kip1 and c-Myc was analyzed by quantitative PCR (qPCR). The level of p27 (Kip1) protein expression was measured by Western blot and the Annexin V method was carried out to investigate apoptosis.
Results:
Flow cytometric analysis results of K562 cells transfected with pLenti-III-pre mir155-GFP construct showed a significant increase in cell apoptosis. Gene expression and protein level of p27kip1 were upregulated. However, there was no change in c-Myc expression profile.
Conclusion:
miR-155 could be a promising approach to aid in the treatment of CML. However, further studies are required in this respect.
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Submitted: 25 Dec 2016
Revision: 29 Mar 2017
Accepted: 08 Apr 2017
ePublished: 26 Apr 2017
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