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CC BY-NC-ND 4.0 · Arq Neuropsiquiatr 2017; 75(12): 875-880
DOI: 10.1590/0004-282X20170156
Article

High expression of XIAP and Bcl-2 may inhibit programmed cell death in glioblastomas

Alta expressão de XIAP e Bcl-2 pode inibir morte celular programada em glioblastomas
Daniela Pretti da Cunha Tirapelli
1   Universidade de São Paulo, Departamento de Cirurgia e Anatomia, Ribeirão Preto SP, Brasil
,
Isis Lacrose Lustosa
1   Universidade de São Paulo, Departamento de Cirurgia e Anatomia, Ribeirão Preto SP, Brasil
,
Sarah Bomfim Menezes
1   Universidade de São Paulo, Departamento de Cirurgia e Anatomia, Ribeirão Preto SP, Brasil
,
Indira Maynart Franco
1   Universidade de São Paulo, Departamento de Cirurgia e Anatomia, Ribeirão Preto SP, Brasil
,
Andressa Romualdo Rodrigues
1   Universidade de São Paulo, Departamento de Cirurgia e Anatomia, Ribeirão Preto SP, Brasil
,
Fernanda Maris Peria
2   Universidade de São Paulo, Departamento de Medicina Interna, Ribeirão Preto SP, Brasil
,
Alexandre Magno da Nóbrega Marinho
3   Universidade Federal de Campina Grande, Unidade Acadêmica de Ciências Médicas, Campina Grande PB, Brazil
,
Luciano Neder Serafini
4   Universidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Departamento de Patologia e Medicina Legal, Ribeirão Preto SP, Brasil
,
Carlos Gilberto Carlotti Jr
1   Universidade de São Paulo, Departamento de Cirurgia e Anatomia, Ribeirão Preto SP, Brasil
,
Luís Fernando Tirapelli
1   Universidade de São Paulo, Departamento de Cirurgia e Anatomia, Ribeirão Preto SP, Brasil
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ABSTRACT

Glioblastoma (GBM) is the most malignant glioma and represents 29% of all brain tumors. Tumorigenesis is intimately connected with characteristics acquired in the physiologic pathway of cellular death.

Objective: In the present study, the expression of anti-apoptotic (XIAP and Bcl-2) and apoptotic (cytochrome C, caspase 9, APAF-1), caspase 3 and the Smac/DIABLO genes related to the apoptosis pathway were evaluated in 30 samples of glioblastoma.

Methods: The gene expression was evaluated in 30 glioblastomas (WHO grade IV) and compared to 10 white matter control samples with real-time PCR.

Results and Conclusion: There were higher expressions of XIAP (p = 0.0032) and Bcl-2 (p = 0.0351) in the glioblastoma samples compared to the control samples of normal brain. These results raise the question of whether Bcl-2 and XIAP genes can be responsible for the inhibition of programmed cell death in glioblastomas. Moreover, they provide additional information capable of allowing the development of new target therapy strategies.

RESUMO

O glioblastoma (GBM) é o glioma mais maligno e representa 29% de todos os tumores cerebrais. A tumorigênese está intimamente ligada à características adquiridas na via fisiológica de morte celular.

Objetivo: Avaliar a expressão de genes anti-apoptóticos (XIAP e Bcl-2) e apoptóticos (citocromo C, a caspase 9, APAF-1), caspase 3 e SMAC/DIABLO, relacionados à apoptose, em 30 amostras de tecido de pacientes com glioblastoma.

Métodos: A expressão gênica foi avaliada em trinta glioblastomas e comparada a dez amostras controles de substância branca por PCR em tempo real.

Resultados e Conclusão: Houve maior nível de expressão de XIAP (p = 0,0032) e Bcl-2 (p = 0,0351) em comparação com as amostras controle, de cérebro normal. Estes resultados levantam a questão de que os genes Bcl-2 e XIAP podem ser responsáveis pela inibição da morte celular programada em glioblastomas, além disso, proporcionam informação adicional capaz de permitir o desenvolvimento de novas estratégias de terapia alvo.

Keywords:

glioblastoma - apoptosis - X-linked inhibitor of apoptosis protein - B-cell lymphoma 2

Palavras-chave:

glioblastoma - apoptose - proteínas inibidoras de apoptose ligadas ao cromossomo X - célula-B de linfoma 2


Publication History

Received: 11 August 2016

Accepted: 14 August 2017

Article published online:
01 September 2023

© 2023. Academia Brasileira de Neurologia. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commecial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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