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Interactions Among Mitochondrial Proteins Altered in Glioblastoma

Overview
Journal J Neurooncol
Publisher Springer
Date 2014 Apr 15
PMID 24728830
Citations 42
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Abstract

Mitochondrial dysfunction is putatively central to glioblastoma (GBM) pathophysiology but there has been no systematic analysis in GBM of the proteins which are integral to mitochondrial function. Alterations in proteins in mitochondrial enriched fractions from patients with GBM were defined with label-free liquid chromatography mass spectrometry. 256 mitochondrially-associated proteins were identified in mitochondrial enriched fractions and 117 of these mitochondrial proteins were markedly (fold-change ≥ 2) and significantly altered in GBM (p ≤ 0.05). Proteins associated with oxidative damage (including catalase, superoxide dismutase 2, peroxiredoxin 1 and peroxiredoxin 4) were increased in GBM. Protein-protein interaction analysis highlighted a reduction in multiple proteins coupled to energy metabolism (in particular respiratory chain proteins, including 23 complex-I proteins). Qualitative ultrastructural analysis in GBM with electron microscopy showed a notably higher prevalence of mitochondria with cristolysis in GBM. This study highlights the complex mitochondrial proteomic adjustments which occur in GBM pathophysiology.

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References
1.
Cuezva J, Ortega A, Willers I, Sanchez-Cenizo L, Aldea M, Sanchez-Arago M . The tumor suppressor function of mitochondria: translation into the clinics. Biochim Biophys Acta. 2009; 1792(12):1145-58. DOI: 10.1016/j.bbadis.2009.01.006. View

2.
Lupertz R, Chovolou Y, Kampkotter A, Watjen W, Kahl R . Catalase overexpression impairs TNF-alpha induced NF-kappaB activation and sensitizes MCF-7 cells against TNF-alpha. J Cell Biochem. 2007; 103(5):1497-511. DOI: 10.1002/jcb.21538. View

3.
Deighton R, McGregor R, Kemp J, McCulloch J, Whittle I . Glioma pathophysiology: insights emerging from proteomics. Brain Pathol. 2010; 20(4):691-703. PMC: 8094634. DOI: 10.1111/j.1750-3639.2010.00376.x. View

4.
Noh D, Ahn S, Lee R, Kim S, Park I, Chae H . Overexpression of peroxiredoxin in human breast cancer. Anticancer Res. 2001; 21(3B):2085-90. View

5.
Kinnula V, Lehtonen S, Sormunen R, Kaarteenaho-Wiik R, Kang S, Rhee S . Overexpression of peroxiredoxins I, II, III, V, and VI in malignant mesothelioma. J Pathol. 2002; 196(3):316-23. DOI: 10.1002/path.1042. View