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Neurostatin blocks glioma cell cycle progression by inhibiting EGFR activation

Neurostatin blocks glioma cell cycle progression by inhibiting EGFR activation
Neurostatin blocks glioma cell cycle progression by inhibiting EGFR activation
The high frequency and malignancy of human glioblastomas has stimulated the search for potential therapeutic approaches. The control of the glioma cell proliferation in response to mitogenic signals is one of the most promising antitumoral strategies, and the main target of several therapies. Neurostatin, an O-acetylated derivative of the ganglioside GD1b, has potent antiproliferative activity over the in vitro and in vivo growth of glioma cells. The mechanism of its antitumoral action is the focus of the present study. Using a combined in vitro-in vivo approach, we observed that neurostatin arrested glioma proliferation by inhibiting the expression of cell cycle promoters (i.e. cyclins and CDKs) and promoting the expression of cell cycle inhibitors (i.e. p21 and p27). Neurostatin inhibits epidermal growth factor receptor (EGFR) signaling pathways, blocking the activation of the main promitogenic MAPKs and PI3K pathways. Neurostatin action not only interferes in the cell cycle progression, but also in the protection from apoptosis, and the generation of angiogenic and invasive responses. The antitumoral actions described here point to neurostatin as a novel and promising chemotherapeutic agent for glioma treatment.
1044-7431
89-100
Valle-Argos, Beatriz
4fddaa71-c0aa-4b95-b464-8bdb592428a2
Gomez-Nicola, Diego
0680aa66-9dee-47cf-a8d3-e39c988f85b5
Nieto-Sampedro, Manuel
6d62c63e-e900-4219-b596-447dae4b0c2d
Valle-Argos, Beatriz
4fddaa71-c0aa-4b95-b464-8bdb592428a2
Gomez-Nicola, Diego
0680aa66-9dee-47cf-a8d3-e39c988f85b5
Nieto-Sampedro, Manuel
6d62c63e-e900-4219-b596-447dae4b0c2d

Valle-Argos, Beatriz, Gomez-Nicola, Diego and Nieto-Sampedro, Manuel (2011) Neurostatin blocks glioma cell cycle progression by inhibiting EGFR activation. Molecular and Cellular Neuroscience, 46 (1), 89-100. (doi:10.1016/j.mcn.2010.08.009). (PMID:20801220)

Record type: Article

Abstract

The high frequency and malignancy of human glioblastomas has stimulated the search for potential therapeutic approaches. The control of the glioma cell proliferation in response to mitogenic signals is one of the most promising antitumoral strategies, and the main target of several therapies. Neurostatin, an O-acetylated derivative of the ganglioside GD1b, has potent antiproliferative activity over the in vitro and in vivo growth of glioma cells. The mechanism of its antitumoral action is the focus of the present study. Using a combined in vitro-in vivo approach, we observed that neurostatin arrested glioma proliferation by inhibiting the expression of cell cycle promoters (i.e. cyclins and CDKs) and promoting the expression of cell cycle inhibitors (i.e. p21 and p27). Neurostatin inhibits epidermal growth factor receptor (EGFR) signaling pathways, blocking the activation of the main promitogenic MAPKs and PI3K pathways. Neurostatin action not only interferes in the cell cycle progression, but also in the protection from apoptosis, and the generation of angiogenic and invasive responses. The antitumoral actions described here point to neurostatin as a novel and promising chemotherapeutic agent for glioma treatment.

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More information

e-pub ahead of print date: 27 August 2010
Published date: January 2011
Organisations: Biomedicine

Identifiers

Local EPrints ID: 333248
URI: https://eprints.soton.ac.uk/id/eprint/333248
ISSN: 1044-7431
PURE UUID: d9e8b08d-c75f-43c1-a90a-706e00cf1bc1
ORCID for Diego Gomez-Nicola: ORCID iD orcid.org/0000-0002-5316-2682

Catalogue record

Date deposited: 06 Mar 2012 11:58
Last modified: 06 Jun 2018 12:33

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