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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...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Tabriz University of Medical Sciences
2017
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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. |
format | Online Article Text |
id | pubmed-5524985 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Tabriz University of Medical Sciences |
record_format | MEDLINE/PubMed |
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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