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CD97 gene expression and function correlate with WT1 protein expression and glioma invasiveness
Date:2/7/2012

ously documented WT1 expression in 80% of glioma cells and tumor specimens. Because WT1 expression in tumor cells has been shown to play a role in resistance to radiation and chemotherapy as well as promotion of cell proliferation, invasion, and/or angiogenesis, Dr. Broaddus brought together the team to investigate what genes present in malignant gliomas could be mediated by WT1 to confer the virulence displayed by this particular tumor. According to the authors, "given its structural identityand functional history, it seemed logical that WT1 might regulate the transcription (or posttranscriptional expression) of other genes."

To this end, the research team set out to silence WT1 gene expression in malignant glioma cells and observe the effects of this silencing on other genes in these cells. The researchers did this by using short interfering RNA (siRNA) directed against WT1 in three glioblastoma cell lines: U251-MG, U1242-MG, and GBM-6.

Application of siRNA consistently suppressed WT1 gene expression levels, which in turn produced a significant reduction in cellular invasiveness. A microarray analysis identified other genes that were affected by WT1 silencing. These included 27 genes that were significantly downregulated and 11 that were significantly upregulated. The authors point out that nine of the 27 downregulated genes have putative or established roles in oncogenesis, and seven of the 11 upregulated genes have putative or established roles in tumor suppression. All but one gene demonstrating dysregulation during WT1 silencing have at least one potential binding site for WT1 in their promoter regions; the other gene (PDGF-D) has binding sites for Egr1, which recognizes and binds consensus binding sequences shared by WT1.

Prior to this study, there were no reports of CD97 overexpression in glioma cells. It was therefore surprising to the research team that the CD97 gene consistently displayed a direct correlation with WT1 in all th
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Contact: Gillian Shasby
gshasby@thejns.org
434-924-5555
Journal of Neurosurgery Publishing Group
Source:Eurekalert

Page: 1 2 3

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