miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1
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 f...
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Format: | Article |
Language: | English |
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Tabriz University of Medical Sciences
2017-06-01
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Series: | BioImpacts |
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Online Access: | http://bi.tbzmed.ac.ir/PDF/bi-7-109.pdf |
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author | Mahdi Edalati Fathabad Morteza Karimipoor Shaban Alizadeh Asghar Abdoli Amir Atashi Mahtab Sayadi |
author_facet | Mahdi Edalati Fathabad Morteza Karimipoor Shaban Alizadeh Asghar Abdoli Amir Atashi Mahtab Sayadi |
author_sort | Mahdi Edalati Fathabad |
collection | DOAJ |
description | 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. |
first_indexed | 2024-12-21T15:38:29Z |
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id | doaj.art-524436a4c65443d3801b99a3340b566b |
institution | Directory Open Access Journal |
issn | 2228-5660 2228-5652 |
language | English |
last_indexed | 2024-12-21T15:38:29Z |
publishDate | 2017-06-01 |
publisher | Tabriz University of Medical Sciences |
record_format | Article |
series | BioImpacts |
spelling | doaj.art-524436a4c65443d3801b99a3340b566b2022-12-21T18:58:34ZengTabriz University of Medical SciencesBioImpacts2228-56602228-56522017-06-017210911410.15171/bi.2017.14BI_15980_20161225151423miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1Mahdi Edalati Fathabad0Morteza Karimipoor1Shaban Alizadeh2Asghar Abdoli3Amir Atashi4Mahtab Sayadi5Hematology Department, School of Allied Medicine, Tehran University of Medical Sciences, Tehran, IranMolecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, IranHematology Department, School of Allied Medicine, Tehran University of Medical Sciences, Tehran, IranDepartment of Hepatitis and AIDS, Pasteur Institute of Iran, Tehran, IranCancer Prevention Research Center, Shahroud University of Medical Sciences, Shahroud, IranCancer Prevention Research Center, Shahroud University of Medical Sciences, Shahroud, IranIntroduction: 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.http://bi.tbzmed.ac.ir/PDF/bi-7-109.pdfApoptosisK562miR-155Philadelphiap27kip1 |
spellingShingle | Mahdi Edalati Fathabad Morteza Karimipoor Shaban Alizadeh Asghar Abdoli Amir Atashi Mahtab Sayadi miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1 BioImpacts Apoptosis K562 miR-155 Philadelphia 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 | Apoptosis K562 miR-155 Philadelphia p27kip1 |
url | http://bi.tbzmed.ac.ir/PDF/bi-7-109.pdf |
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