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Genome-wide transcriptional analyses of Chinese patients reveal cell migration is attenuated in IDH1-mutant glioblastomas.
- Source :
-
Cancer letters [Cancer Lett] 2015 Feb 28; Vol. 357 (2), pp. 566-74. Date of Electronic Publication: 2014 Dec 12. - Publication Year :
- 2015
-
Abstract
- Patients with isocitrate dehydrogenase 1 (IDH1)-mutant glioblastoma exhibit increased survival compared with those with wild-type IDH1 tumors. The magnitude of this finding has led to the use of IDH1 mutations as diagnostic and prognostic biomarkers. However, the mechanisms underlying the reported correlation between the IDH1 mutation and increased survival have not been fully revealed. In this work, based on genome-wide transcriptional analyses of 69 Chinese patients with glioblastoma, we have found that the focal adhesion pathway is significantly downregulated in IDH1-mutant glioblastomas. The impaired focal adhesion leads to compromised cell migration and tumor invasion, contributing to the optimistic prognosis of these patients. Moreover, the signature genes of HIF-1α, the downstream factor of mutated IDH1, are found to be suppressed in IDH1-mutant gliomas. Given the role of HIF-1α in cell migration, we conclude that the attenuation of HIF-1α-dependent glioblastoma cell infiltration contributes to the better outcomes of patients with IDH1-mutant gliomas.<br /> (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)
- Subjects :
- Asian People genetics
Cell Line, Tumor
China
Focal Adhesions genetics
Gene Regulatory Networks
Glioblastoma ethnology
Glioblastoma metabolism
HEK293 Cells
Humans
Hypoxia-Inducible Factor 1, alpha Subunit genetics
Hypoxia-Inducible Factor 1, alpha Subunit metabolism
Immunohistochemistry
Isocitrate Dehydrogenase metabolism
Models, Genetic
Oligonucleotide Array Sequence Analysis
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction genetics
Cell Movement genetics
Gene Expression Regulation, Neoplastic
Glioblastoma genetics
Isocitrate Dehydrogenase genetics
Mutation
Transcriptome genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1872-7980
- Volume :
- 357
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Cancer letters
- Publication Type :
- Academic Journal
- Accession number :
- 25511738
- Full Text :
- https://doi.org/10.1016/j.canlet.2014.12.018