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Transcriptional profiling of EGFR variants in mouse Glioblastoma model

ABSTRACT: Transcriptional profiling of EGFR variants in mouse Glioblastoma model

PROVIDER: PRJNA762321 | ENA |

REPOSITORIES: ENA

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Transcriptional profiling of EGFR variants in mouse Glioblastoma model

Project description:The RTK/PI3K/MAPK pathway is one of the most frequently altered pathways in Glioblastoma (GBM) with EGFR mutations and/or amplifications present in 57% of all samples. It remains the most frequently mutated oncogene in GBM. We utilized an established in vivo competition screening assay to identify and validate bona fide, driver mutations in GBM. The screen nominated A298I, T263P, and R108G mutations as potential drivers. We also analyzed R108K and R222C which were not identified by the screen. The goal of this study is to characterize the transcriptional changes of GBM when driven by different EGFR variants. Using in utero electroporation (IUE) and CRISPR/Cas9 constructs we knocked out Tp53 and Pten in developing glial cells. Each EGFR variant was overexpressed in this model and tumors were collected at end stage for RNA-sequencing analysis.

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EGFR pathway expression persists in recurrent glioblastoma independent of amplification status

Project description:Background: Glioblastoma mortality is driven by tumour progression or recurrence despite administering a therapeutic arsenal consisting of surgical resection, radiation, and alkylating chemotherapy. The genetic changes underlying tumour progression and chemotherapy resistance are poorly understood. Methods: In this work, we sought to define the relationship between EGFR amplification status, EGFR mRNA expression, and EGFR pathway activity. We compared RNA-sequencing data from matched primary and recurrent tumour samples (N = 40 patients, 20 with EGFR amplification). Results: In the setting of glioblastoma recurrence, the EGFR pathway was overexpressed regardless of EGFR amplification status, suggesting a common genomic endpoint in recurrent glioblastoma, although EGFR amplification did associate with higher EGFR mRNA expression. Three of forty patients in the study cohort had EGFR-amplified tumours and received targeted EGFR therapy. Their molecular subtypes and clinical outcomes did not significantly differ from patients who received conventional chemotherapy. Conclusion: Our findings suggest that while the EGFR amplification may confer a unique molecular profile in primary glioblastoma, pathway analysis reveals upregulation of the EGFR pathway in recurrence, regardless of amplification status. As such, the EGFR pathway may be a key mediator of glioblastoma progression.

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Project description:Here we have used 4C-seq to interrogate the toplogy of the EGFR locus in glioblastoma models that are EGFR unamplified (GSC23) and amplified (GBM3565).

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Project description:Epidermal Growth Factor Receptor (EGFR) gene amplification and mutations are the most common oncogenic events in Glioblastoma (GBM), but the mechanisms by which they promote aggressive tumor growth are not well understood. Here, through integrated epigenome and transcriptome analyses of cell lines, genotyped clinical samples and TCGA data, we show that EGFR mutations remodel the activated enhancer landscape of GBM, promoting tumorigenesis through a SOX9 and FOXG1-dependent transcriptional regulatory network in vitro and in vivo. The most common EGFR mutation, EGFRvIII, sensitizes GBM cells to the BET-bromodomain inhibitor JQ1 in a SOX9, FOXG1-dependent manner. These results identify the role of transcriptional/epigenetic remodeling in EGFR-dependent pathogenesis and suggest a mechanistic basis for epigenetic therapy. ChIP-Seq for H3K27ac, H3K4me1, and H3K4me3, and RNA-seq for Glioblastoma (GBM) cells and/or tissues with or without EGFRvIII mutation.

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Project description:The RNA-binding protein Transformer 2 alpha homolog (TRA2A), previously identified as an alternative splicing factor, was reported as a crucial oncogene in recent years. However, the underlying mechanisms are poorly understood. In this study, we found that TRA2A is highly up-regulated in glioblastoma and is significantly correlated with clinical diagnosis and prognosis. We verified that TRA2A promotes the proliferation and metastasis of glioblastoma. Epitranscriptomic profiling further revealed Interferon-induced protein with tetratricopeptide repeat 1/2/3 (IFIT1/2//3) as the key RNA targets mediated by TRA2A, which further over-activates the EGFR-AKT signaling pathway by enhancing the recycling of p-EGFR. This work reveals a novel oncogenic mechanism of TRA2A in glioblastoma.

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