Event Title

The Role of DNA Methylation in Different Subtypes of Glioblastoma

Session Number

C18

Advisor(s)

Shi-Yuan Cheng, Northwestern University
Rajendra Pangeni, Northwestern University

Location

B-131 Grainger

Start Date

28-4-2016 12:45 PM

End Date

28-4-2016 1:10 PM

Disciplines

Biology

Abstract

DNA methylation, a mechanism that regulates gene expression, is associated with various cancers including glioblastoma (GBM). The purpose of this investigation was to investigate the role of DNA methylation in GBM stem cell (GSC) subtypes including mainly proneural (PN) and mesenchymal (MES). We carried out 450K methylation array on the GSCs to obtain levels of methylation and used gene expression data sets to obtain gene expression. We compared and found corresponding methylation and gene expression to identify candidate genes and validated the gene expression through quantitative reverse transcription polymerase chain reaction and Western blot. Out of the candidate genes, further work was done to specific genes due to their dysregulated methylation in MES and non-methylation in PN which corresponded to the high level of gene expression in PN and low level of gene expression in MES. The results suggested that DNA methylation does play a role in PN and MES GSCs phenotypes and their tumorigenic properties. This investigation could possibly help further in understanding DNA methylation associated with phenotypes of malignant GBMs and lead to more specific therapeutic targets.


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Apr 28th, 12:45 PM Apr 28th, 1:10 PM

The Role of DNA Methylation in Different Subtypes of Glioblastoma

B-131 Grainger

DNA methylation, a mechanism that regulates gene expression, is associated with various cancers including glioblastoma (GBM). The purpose of this investigation was to investigate the role of DNA methylation in GBM stem cell (GSC) subtypes including mainly proneural (PN) and mesenchymal (MES). We carried out 450K methylation array on the GSCs to obtain levels of methylation and used gene expression data sets to obtain gene expression. We compared and found corresponding methylation and gene expression to identify candidate genes and validated the gene expression through quantitative reverse transcription polymerase chain reaction and Western blot. Out of the candidate genes, further work was done to specific genes due to their dysregulated methylation in MES and non-methylation in PN which corresponded to the high level of gene expression in PN and low level of gene expression in MES. The results suggested that DNA methylation does play a role in PN and MES GSCs phenotypes and their tumorigenic properties. This investigation could possibly help further in understanding DNA methylation associated with phenotypes of malignant GBMs and lead to more specific therapeutic targets.