Understanding the Biological Basis of Glioblastoma Patient-derived Spheroids.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Mar 2021
Historique:
received: 16 12 2020
revised: 24 01 2021
accepted: 26 01 2021
entrez: 31 3 2021
pubmed: 1 4 2021
medline: 13 4 2021
Statut: ppublish

Résumé

Resistance to glioblastoma (GB) therapy is attributed to the presence of glioblastoma stem cells (GSC). Here, we defined the behavior of GSC as it pertains to proliferation, migration, and angiogenesis. Human-derived GSC were isolated and cultured from GB patient tumors. Xenograft GSC were extracted from the xenograft tumors, and spheroids were created and compared with human GSC spheroids by flow cytometry, migration, proliferation, and angiogenesis assays. Oct3/4 and Sox2, GFAP, and Ku80 expression was assessed by immunoanalysis. The xenograft model showed the formation of two different tumors with distinct characteristics. Tumors formed at 2 weeks were less aggressive with well-defined margins, whereas tumors formed in 5 months were diffuse and aggressive. Expression of Oct3/4 and Sox2 was positive in both human and xenograft GSC. Positive Ku80 expression in xenograft GSC confirmed their human origin. Human and xenograft GSC migrated vigorously in collagen and Matrigel, respectively. Xenograft GSC displayed a higher rate of migration and invasion than human GSC. Human GSC were more aggressive in growth and proliferation than xenograft GSC, while xenograft GSC had increased invasion and migration compared to human GSC. A simple in vitro spheroid system for GSC provides a superior platform for the development of precision medicine in the treatment of GB.

Sections du résumé

BACKGROUND/AIM OBJECTIVE
Resistance to glioblastoma (GB) therapy is attributed to the presence of glioblastoma stem cells (GSC). Here, we defined the behavior of GSC as it pertains to proliferation, migration, and angiogenesis.
MATERIALS AND METHODS METHODS
Human-derived GSC were isolated and cultured from GB patient tumors. Xenograft GSC were extracted from the xenograft tumors, and spheroids were created and compared with human GSC spheroids by flow cytometry, migration, proliferation, and angiogenesis assays. Oct3/4 and Sox2, GFAP, and Ku80 expression was assessed by immunoanalysis.
RESULTS RESULTS
The xenograft model showed the formation of two different tumors with distinct characteristics. Tumors formed at 2 weeks were less aggressive with well-defined margins, whereas tumors formed in 5 months were diffuse and aggressive. Expression of Oct3/4 and Sox2 was positive in both human and xenograft GSC. Positive Ku80 expression in xenograft GSC confirmed their human origin. Human and xenograft GSC migrated vigorously in collagen and Matrigel, respectively. Xenograft GSC displayed a higher rate of migration and invasion than human GSC.
CONCLUSION CONCLUSIONS
Human GSC were more aggressive in growth and proliferation than xenograft GSC, while xenograft GSC had increased invasion and migration compared to human GSC. A simple in vitro spheroid system for GSC provides a superior platform for the development of precision medicine in the treatment of GB.

Identifiants

pubmed: 33788709
pii: 41/3/1183
doi: 10.21873/anticanres.14875
doi:

Substances chimiques

AC133 Antigen 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1183-1195

Informations de copyright

Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Karolína Turnovcova (K)

Department of Neuroregeneration Institute of Experimental Medicine Czech Academy of Science, Prague, Czech Republic.

Dana Marekova (D)

Department of Neuroregeneration Institute of Experimental Medicine Czech Academy of Science, Prague, Czech Republic.
Second Faculty of Medicine, Charles University, Prague, Czech Republic.

Tolga Sursal (T)

Department of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY, U.S.A.

Marketa Krupova (M)

The Fingerland Department of Pathology, Faculty of Medicine and University Hospital in Hradec Kralové, Charles University, Hradec Kralové, Czech Republic.

Ronan Gandhi (R)

Department of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY, U.S.A.

Petr Krupa (P)

Department of Neuroregeneration Institute of Experimental Medicine Czech Academy of Science, Prague, Czech Republic.
Department of Neurosurgery Faculty of Medicine and University Hospital in Hradec Kralove, Charles University, Hradec Kralove, Czech Republic.

Radek Kaiser (R)

Department of Neurosurgery and Neurooncology, First Faculty of Medicine, Charles University and Military University Hospital, Prague, Czech Republic.

Vit Herynek (V)

Center for Advanced Preclinical Imaging, First Faculty of Medicine, Charles University, Prague, Czech Republic.

David Netuka (D)

Department of Neurosurgery and Neurooncology, First Faculty of Medicine, Charles University and Military University Hospital, Prague, Czech Republic.

Pavla Jendelova (P)

Department of Neuroregeneration Institute of Experimental Medicine Czech Academy of Science, Prague, Czech Republic; pavla.jendelova@iem.cas.cz meena_jhanwar@nymc.edu.
Second Faculty of Medicine, Charles University, Prague, Czech Republic.

Meena Jhanwar-Uniyal (M)

Department of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY, U.S.A.

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Classifications MeSH