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Potential identity of multi-potential cancer stem-like subpopulation after radiation of cultured brain glioma

BACKGROUND: Glioblastoma multiforme (GBM) is the most frequently encountered brain cancer. Although the existence of cancer stem cells in GBM has been previously established, there is little evidence to explain the difference between cancer stem cells and radio-resistant cells in GBM. In an effort t...

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Autores principales: Kang, Mi K, Hur, Beong I, Ko, Mi H, Kim, Cheul H, Cha, Seung H, Kang, Soo K
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2266936/
https://www.ncbi.nlm.nih.gov/pubmed/18230189
http://dx.doi.org/10.1186/1471-2202-9-15
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author Kang, Mi K
Hur, Beong I
Ko, Mi H
Kim, Cheul H
Cha, Seung H
Kang, Soo K
author_facet Kang, Mi K
Hur, Beong I
Ko, Mi H
Kim, Cheul H
Cha, Seung H
Kang, Soo K
author_sort Kang, Mi K
collection PubMed
description BACKGROUND: Glioblastoma multiforme (GBM) is the most frequently encountered brain cancer. Although the existence of cancer stem cells in GBM has been previously established, there is little evidence to explain the difference between cancer stem cells and radio-resistant cells in GBM. In an effort to increase our understanding of whether cellular radio-resistance is a characteristic associated with cancer stem cells, we developed a dissociated cell system of subpopulations derived from GBM, and demonstrated radiotherapy resistance therein. RESULTS: The radio-resistant cancer cell subpopulations of GBM abundantly express CD133, CD117, CD71, and CD45 surface markers, and these radio-resistant cancer cell subpopulations have the capacity for extensive proliferation, self-renewal, and pluripotency. These radio-resistant cancer subpopulations have been shown to initiate tumorigenesis when transplanted into SCID mouse brains. Moreover, these tumors evidenced highly peculiar nest-like shapes harboring both vascular and cancerous tissue structures, which expressed the blood vessel specific marker, the von Willebrand factor. Accordingly, subpopulations of radio-resistant cells in GBM have been shown to be very similar to hematopoietic stem cells (HSCs) in the circulating blood. This similarity may contribute to increased tumor growth and GBM recurrence. CONCLUSION: The results of the present study provide further evidence for radio resistant subpopulations of cancer stem cells in GBM. Also, our results will assist in the identification and characterization of cancer stem cell populations in glioma, and will help to improve the therapeutic outcomes of GBM.
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spelling pubmed-22669362008-03-12 Potential identity of multi-potential cancer stem-like subpopulation after radiation of cultured brain glioma Kang, Mi K Hur, Beong I Ko, Mi H Kim, Cheul H Cha, Seung H Kang, Soo K BMC Neurosci Research Article BACKGROUND: Glioblastoma multiforme (GBM) is the most frequently encountered brain cancer. Although the existence of cancer stem cells in GBM has been previously established, there is little evidence to explain the difference between cancer stem cells and radio-resistant cells in GBM. In an effort to increase our understanding of whether cellular radio-resistance is a characteristic associated with cancer stem cells, we developed a dissociated cell system of subpopulations derived from GBM, and demonstrated radiotherapy resistance therein. RESULTS: The radio-resistant cancer cell subpopulations of GBM abundantly express CD133, CD117, CD71, and CD45 surface markers, and these radio-resistant cancer cell subpopulations have the capacity for extensive proliferation, self-renewal, and pluripotency. These radio-resistant cancer subpopulations have been shown to initiate tumorigenesis when transplanted into SCID mouse brains. Moreover, these tumors evidenced highly peculiar nest-like shapes harboring both vascular and cancerous tissue structures, which expressed the blood vessel specific marker, the von Willebrand factor. Accordingly, subpopulations of radio-resistant cells in GBM have been shown to be very similar to hematopoietic stem cells (HSCs) in the circulating blood. This similarity may contribute to increased tumor growth and GBM recurrence. CONCLUSION: The results of the present study provide further evidence for radio resistant subpopulations of cancer stem cells in GBM. Also, our results will assist in the identification and characterization of cancer stem cell populations in glioma, and will help to improve the therapeutic outcomes of GBM. BioMed Central 2008-01-30 /pmc/articles/PMC2266936/ /pubmed/18230189 http://dx.doi.org/10.1186/1471-2202-9-15 Text en Copyright © 2008 Kang et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Kang, Mi K
Hur, Beong I
Ko, Mi H
Kim, Cheul H
Cha, Seung H
Kang, Soo K
Potential identity of multi-potential cancer stem-like subpopulation after radiation of cultured brain glioma
title Potential identity of multi-potential cancer stem-like subpopulation after radiation of cultured brain glioma
title_full Potential identity of multi-potential cancer stem-like subpopulation after radiation of cultured brain glioma
title_fullStr Potential identity of multi-potential cancer stem-like subpopulation after radiation of cultured brain glioma
title_full_unstemmed Potential identity of multi-potential cancer stem-like subpopulation after radiation of cultured brain glioma
title_short Potential identity of multi-potential cancer stem-like subpopulation after radiation of cultured brain glioma
title_sort potential identity of multi-potential cancer stem-like subpopulation after radiation of cultured brain glioma
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2266936/
https://www.ncbi.nlm.nih.gov/pubmed/18230189
http://dx.doi.org/10.1186/1471-2202-9-15
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