Volume 33, Issue 11 p. 1160-1167
RESEARCH ARTICLE

Effects of aloe emodin on U87MG glioblastoma cell growth: In vitro and in vivo study

Antonietta Arcella

Corresponding Author

Antonietta Arcella

IRCCS NEUROMED, Pozzilli, Italy

Antonietta Arcella and Maria Antonietta Oliva contributed equally to this study.Correspondence Antonietta Arcella, IRCCS NEUROMED, Pozzilli, Italy. Email: [email protected]Search for more papers by this author
Maria Antonietta Oliva

Maria Antonietta Oliva

IRCCS NEUROMED, Pozzilli, Italy

Antonietta Arcella and Maria Antonietta Oliva contributed equally to this study.Search for more papers by this author
Sabrina Staffieri

Sabrina Staffieri

IRCCS NEUROMED, Pozzilli, Italy

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Massimo Sanchez

Massimo Sanchez

Istituto Superiore di Sanità, Rome, Italy

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Michele Madonna

Michele Madonna

IRCCS NEUROMED, Pozzilli, Italy

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Barbara Riozzi

Barbara Riozzi

IRCCS NEUROMED, Pozzilli, Italy

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Vincenzo Esposito

Vincenzo Esposito

IRCCS NEUROMED, Pozzilli, Italy

University of Rome “Sapienza”, Rome, Italy

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Felice Giangaspero

Felice Giangaspero

IRCCS NEUROMED, Pozzilli, Italy

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Luigi Frati

Luigi Frati

IRCCS NEUROMED, Pozzilli, Italy

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First published: 15 September 2018
Citations: 24

Abstract

Glioblastoma, the most aggressive and malignant form of glioma, appears to be resistant to various chemotherapeutic agents. Hence other approaches have been investigated to target more pathways involved in glioblastoma development and progression. Here we investigate the anticancer effect of Aloe-Emodin (AE), an anthraquinone compound presents in the leaves of Aloe arborescens, on human glioblastoma cell line U87MG. U87MG were treated with various concentrations of AE (20 and 40 μM) for different times (24, 48, and 72 hr). Cell growth was monitored by daily cell count after treatments. Growth analysis showed that AE significantly decrease proliferation of U87MG in a time and dose dependent manner. FACS analysis demonstrates a block of cell cycle in S and G2/M phase. AE probably induced also apoptosis by releasing of apoptosis-inducing factor: PARP and Lamin activation leading to nuclear shrinkage. In addition, exposure of U87MG to AE reduced pAKT phosphorylation. AE inhibition of U87MG growth is a result of more mechanism together. Here we report that AE has a specific growth inhibition on U87MG also in in vivo. The growth of U87MG, subcutaneously injected in nude mice with severe combined immunodeficiency, is inhibited without any appreciable toxic effects on the animals after AE treatment. AE might represent a conceptually new lead antitumor adjuvant drug.

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