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Matteucinol, isolated from Miconia chamissois, induces apoptosis in human glioblastoma lines via the intrinsic pathway and inhibits angiogenesis and tumor growth in vivo

Authors :
Allisson Rodrigues Rezende
Renato Oliveira
Rosy Iara Maciel de Azambuja Ribeiro
Ralph Gruppi Thomé
Rafael César Russo Chagas
Hélio Batista dos Santos
Wanderson Romão
Viviane Aline Oliveira Silva
Lúcia Pinheiro Santos Pimenta
Ana Gabriela Silva
Rui Manuel Reis
Source :
Investigational New Drugs. 38:1044-1055
Publication Year :
2019
Publisher :
Springer Science and Business Media LLC, 2019.

Abstract

Gliomas account for nearly 70% of the central nervous system tumors and present a median survival of approximately 12-17 months. Studies have shown that administration of novel natural antineoplastic agents is been highly effective for treating gliomas. This study was conducted to investigate the antitumor potential (in vitro and in vivo) of Miconia chamissois Naudin for treating glioblastomas. We investigated the cytotoxicity of the chloroform partition and its sub-fraction in glioblastoma cell lines (GAMG and U251MG) and one normal cell line of astrocytes. The fraction showed cytotoxicity and was selective for tumor cells. Characterization of this fraction revealed a single compound, Matteucinol, which was first identified in the species M. chamissois. Matteucinol promoted cell death via intrinsic apoptosis in the adult glioblastoma lines. In addition, Matteucinol significantly reduced the migration, invasion, and clonogenicity of the tumor cells. Notably, it also reduced tumor growth and angiogenesis in vivo. Moreover, this agent showed synergistic effects with temozolomide, a chemotherapeutic agent commonly used in clinical practice. Our study demonstrates that Matteucinol from M chamissois is a promising compound for the treatment of glioblastomas and may be used along with the existing chemotherapeutic agents for more effective treatment.

Details

ISSN :
15730646 and 01676997
Volume :
38
Database :
OpenAIRE
Journal :
Investigational New Drugs
Accession number :
edsair.doi.dedup.....ba69adbf05cec67564f551ef78aec2fb