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

[Image: see text] 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 ca...

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Autores principales: Edalati Fathabad, Mahdi, Karimipoor, Morteza, Alizadeh, Shaban, Abdoli, Asghar, Atashi, Amir, Sayadi, Mahtab
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Tabriz University of Medical Sciences 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5524985/
https://www.ncbi.nlm.nih.gov/pubmed/28752075
http://dx.doi.org/10.15171/bi.2017.14
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author Edalati Fathabad, Mahdi
Karimipoor, Morteza
Alizadeh, Shaban
Abdoli, Asghar
Atashi, Amir
Sayadi, Mahtab
author_facet Edalati Fathabad, Mahdi
Karimipoor, Morteza
Alizadeh, Shaban
Abdoli, Asghar
Atashi, Amir
Sayadi, Mahtab
author_sort Edalati Fathabad, Mahdi
collection PubMed
description [Image: see text] 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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spelling pubmed-55249852017-07-27 miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1 Edalati Fathabad, Mahdi Karimipoor, Morteza Alizadeh, Shaban Abdoli, Asghar Atashi, Amir Sayadi, Mahtab Bioimpacts Original Research [Image: see text] 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. Tabriz University of Medical Sciences 2017 2017-04-26 /pmc/articles/PMC5524985/ /pubmed/28752075 http://dx.doi.org/10.15171/bi.2017.14 Text en © 2017 The Author(s) This work is published by BioImpacts as an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/). Non-commercial uses of the work are permitted, provided the original work is properly cited.
spellingShingle Original Research
Edalati Fathabad, Mahdi
Karimipoor, Morteza
Alizadeh, Shaban
Abdoli, Asghar
Atashi, Amir
Sayadi, Mahtab
miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1
title miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1
title_full miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1
title_fullStr miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1
title_full_unstemmed miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1
title_short miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1
title_sort mir-155 effectively induces apoptosis in k562 philadelphia positive cell line through upregulation of p27kip1
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5524985/
https://www.ncbi.nlm.nih.gov/pubmed/28752075
http://dx.doi.org/10.15171/bi.2017.14
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