Biochemical and Biophysical Research Communications
Proteomics-based identification of differentially expressed genes in human gliomas: down-regulation of SIRT2 gene
Section snippets
Materials and methods
Brain tissues. Brain tumor tissues and non-tumor tissues were obtained from Tottori University Hospital with informed consent and approved by an Institutional Review Committee. Tissues were flash-frozen in liquid nitrogen immediately after surgical removal and stored at −80 °C. Diagnosis of glioma was confirmed histopathologically. Gliomas were then classified according to the WHO grading scheme for central nervous system tumors [8].
Cell culture, transfection of EGFP-SIRT2 expression plasmid,
2D gel separation of proteins
Glioma tissues derived from five individuals were classified according to the WHO grading system for central nervous system tumors. In this study, gliomas classified as grade II (G201), III (G301 and G302), and IV (G402 and G405) were processed for 2D electrophoresis to isolate candidate proteins that are differentially regulated in gliomas. We detected about 1000 protein spots on the 2D gels after SYPRO Ruby staining (Fig. 1). The 2D electrophoresis profiles and relative spot intensities
Discussion
In this study, we analyzed differentially expressed proteins in human gliomas using a proteomics-based approach. To our knowledge, this is the first report of the use of a proteomics-based approach for the study of human gliomas.
We identified 11 proteins that are overexpressed and four proteins that are down-regulated in this type of cancer. One of the down-regulated proteins was identified as SIRT2 tubulin deacetylase which is located on 19q13.2, a region whose frequent deletion in gliomas was
Acknowledgements
We thank M. Kameyama, H. Yamada, and I. Kishimoto for technical assistance. We also thank R. Nishigaki for computing assistance. This work was supported in part by grants from the Ministry of Health, Labour and Welfare and the Ministry of Education, Culture, Sports, Science and Technology of Japan. C.G.T.T. is supported by the Japanese Government (Monbukagakusho) Scholarship.
References (26)
- et al.
GOA, a novel gene encoding a ring finger B-box coiled-coil protein, is overexpressed in astrocytoma
Biochem. Biophys. Res. Commun.
(2001) - et al.
An extra human chromosome 21 reduces mlc-2a expression in chimeric mice and Down syndrome
Biochem. Biophys. Res. Commun.
(2002) - et al.
PEA-15 mediates cytoplasmic sequestration of ERK MAP kinase
Dev. Cell
(2001) - et al.
Prohibitin gene is overexpressed but not mutated in rat bladder carcinomas and cell lines
Cancer Lett.
(1994) - et al.
The human Sir2 ortholog, SIRT2, is an NAD+-dependent tubulin deacetylase
Mol. Cell
(2003) - et al.
Centromeres and kinetochores: from epigenetics to mitotic checkpoint signaling
Cell
(2003) - et al.
Evidence that collapsin response mediator protein-2 is involved in the dynamics of microtubules
J. Biol. Chem.
(2000) - et al.
Neurocalcin–actin interaction
Biochim. Biophys. Acta
(2001) - et al.
Isolation and characterization of genes associated with the anti-tumor activity of glucocorticoids
Brain Res. Mol. Brain Res.
(2002) - et al.
The functional role of tumor suppressor genes in gliomas: clues for future therapeutic strategies
Neurology
(1998)
Molecular pathogenesis of malignant gliomas
Curr. Opin. Oncol.
Deletion mapping of chromosome 19 in human gliomas
Int. J. Cancer
Genes differentially expressed in medulloblastoma and fetal brain
Physiol. Genomics
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