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Mesenchymal Stem Cells cause Telomere Length Reduction of Molt-4 Cells via Caspase-3, BAD and P53 Apoptotic Pathway
Mesenchymal stem cells (MSCs) as undifferentiated cells are specially considered in cell-based cancer therapy due to unique features such as multi-potency, pluripotency, and self-renewal. A multitude of cytokines secreted from MSCs are known to give such multifunctional attributes, but details of th...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Babol University of Medical Sciences
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8496249/ https://www.ncbi.nlm.nih.gov/pubmed/34703795 http://dx.doi.org/10.22088/IJMCM.BUMS.10.2.113 |
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author | Heidari, Hamid Reza Fathi, Ezzatollah Montazersaheb, Soheila Mamandi, Ayoub Farahzadi, Raheleh Zalavi, Soran Nozad Charoudeh, Hojjatollah |
author_facet | Heidari, Hamid Reza Fathi, Ezzatollah Montazersaheb, Soheila Mamandi, Ayoub Farahzadi, Raheleh Zalavi, Soran Nozad Charoudeh, Hojjatollah |
author_sort | Heidari, Hamid Reza |
collection | PubMed |
description | Mesenchymal stem cells (MSCs) as undifferentiated cells are specially considered in cell-based cancer therapy due to unique features such as multi-potency, pluripotency, and self-renewal. A multitude of cytokines secreted from MSCs are known to give such multifunctional attributes, but details of their role are yet to be unknown. In the present study, MSCs were cultured, characterized and co-cultured with Molt-4 cells as acute lymphoblastic leukemia cell line in a trans-well plate. Then, cultured Molt-4 alone and Molt-4 co-cultured with MSCs (10:1) were collected on day 7 and subjected to real time-PCR and Western blotting for gene and protein expression assessment, respectively. Ki-67/caspase-3 as well as telomere length were investigated by flow cytometry and real time-PCR, respectively. The results showed that MSCs caused significant decrease in telomere length as well as hTERT gene expression of Molt-4 cells. Also, gene and protein expression of BAD and P53 were significantly increased. Furthermore, the flow cytometry analysis indicated the decrease and increase of the Ki-67 and caspaspase-3 expression, respectively. It was concluded that MSCs co-cultured with Molt-4 cells could be involved in the promotion of Molt-4 cell apoptosis via caspase-3, BAD, and P53 expression. In addition, the decrease of telomere length is another effect of MSCs on Molt-4 leukemic cells. |
format | Online Article Text |
id | pubmed-8496249 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Babol University of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-84962492021-10-25 Mesenchymal Stem Cells cause Telomere Length Reduction of Molt-4 Cells via Caspase-3, BAD and P53 Apoptotic Pathway Heidari, Hamid Reza Fathi, Ezzatollah Montazersaheb, Soheila Mamandi, Ayoub Farahzadi, Raheleh Zalavi, Soran Nozad Charoudeh, Hojjatollah Int J Mol Cell Med Original Article Mesenchymal stem cells (MSCs) as undifferentiated cells are specially considered in cell-based cancer therapy due to unique features such as multi-potency, pluripotency, and self-renewal. A multitude of cytokines secreted from MSCs are known to give such multifunctional attributes, but details of their role are yet to be unknown. In the present study, MSCs were cultured, characterized and co-cultured with Molt-4 cells as acute lymphoblastic leukemia cell line in a trans-well plate. Then, cultured Molt-4 alone and Molt-4 co-cultured with MSCs (10:1) were collected on day 7 and subjected to real time-PCR and Western blotting for gene and protein expression assessment, respectively. Ki-67/caspase-3 as well as telomere length were investigated by flow cytometry and real time-PCR, respectively. The results showed that MSCs caused significant decrease in telomere length as well as hTERT gene expression of Molt-4 cells. Also, gene and protein expression of BAD and P53 were significantly increased. Furthermore, the flow cytometry analysis indicated the decrease and increase of the Ki-67 and caspaspase-3 expression, respectively. It was concluded that MSCs co-cultured with Molt-4 cells could be involved in the promotion of Molt-4 cell apoptosis via caspase-3, BAD, and P53 expression. In addition, the decrease of telomere length is another effect of MSCs on Molt-4 leukemic cells. Babol University of Medical Sciences 2021 2021-09-01 /pmc/articles/PMC8496249/ /pubmed/34703795 http://dx.doi.org/10.22088/IJMCM.BUMS.10.2.113 Text en https://creativecommons.org/licenses/by/3.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/ (https://creativecommons.org/licenses/by/3.0/) ) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Heidari, Hamid Reza Fathi, Ezzatollah Montazersaheb, Soheila Mamandi, Ayoub Farahzadi, Raheleh Zalavi, Soran Nozad Charoudeh, Hojjatollah Mesenchymal Stem Cells cause Telomere Length Reduction of Molt-4 Cells via Caspase-3, BAD and P53 Apoptotic Pathway |
title | Mesenchymal Stem Cells cause Telomere Length Reduction of Molt-4 Cells via Caspase-3, BAD and P53 Apoptotic Pathway |
title_full | Mesenchymal Stem Cells cause Telomere Length Reduction of Molt-4 Cells via Caspase-3, BAD and P53 Apoptotic Pathway |
title_fullStr | Mesenchymal Stem Cells cause Telomere Length Reduction of Molt-4 Cells via Caspase-3, BAD and P53 Apoptotic Pathway |
title_full_unstemmed | Mesenchymal Stem Cells cause Telomere Length Reduction of Molt-4 Cells via Caspase-3, BAD and P53 Apoptotic Pathway |
title_short | Mesenchymal Stem Cells cause Telomere Length Reduction of Molt-4 Cells via Caspase-3, BAD and P53 Apoptotic Pathway |
title_sort | mesenchymal stem cells cause telomere length reduction of molt-4 cells via caspase-3, bad and p53 apoptotic pathway |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8496249/ https://www.ncbi.nlm.nih.gov/pubmed/34703795 http://dx.doi.org/10.22088/IJMCM.BUMS.10.2.113 |
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