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RNA-binding protein TRA2A promotes glioblastoma by mediating m6A RNA modification of IFITs to recycle p-EGFR

ABSTRACT: RNA-binding protein TRA2A promotes glioblastoma by mediating m6A RNA modification of IFITs to recycle p-EGFR

PROVIDER: PRJNA1060727 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27412064_1.fastq.gz	Fastqsanger.gz
	SRR27412064_2.fastq.gz	Fastqsanger.gz
	SRR27412065_1.fastq.gz	Fastqsanger.gz
	SRR27412065_2.fastq.gz	Fastqsanger.gz
	SRR27412066_1.fastq.gz	Fastqsanger.gz

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RNA-binding protein TRA2A promotes glioblastoma by mediating m6A RNA modification of IFITs to recycle p-EGFR

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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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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EGFR Mutation Promotes Glioblastoma Through Epigenome and Transcription Factor Network Remodeling

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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EGFR/Src/Erk-Stabilized YTHDF2 Promotes Cholesterol Dysregulation and Invasive Growth of Glioblastoma [RNA-Seq]

Project description:Epidermal growth factor receptor (EGFR) signaling is constitutively activated in majority of GBM and is associated with a worse prognosis. Here we show that EGFR is responsible for overexpression of the m6A "reader" YTHDF2 in GBM through the EGFR/Src/ERK signaling pathway. YTHDF2 overexpression clinically correlates with poor glioma patient prognosis. EGFR signaling stabilizes YTHDF2 protein through phosphorylation of YTHDF2 serine 39 and threonine 381 by ERK1/2. YTHDF2 is required for GBM cell proliferation, invasion and tumorigenesis. YTHDF2 facilitates m6A-dependent mRNA decay of LXRA and HIVEP2, both are genes impacting glioma patient survival. YTHDF2 promotes tumorigenesis of GBM cells largely through downregulation of LXRA and HIVEP2. Further, YTHDF2 inhibits LXRA-dependent cholesterol homeostasis in GBM cells. Together, our findings extend the landscape of EGFR downstream circuit, uncover novel function for YTHDF2 in GBM tumorigenesis, and highlight an essential role of RNA m6A methylation in cholesterol homeostasis.

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EGFR-targeted therapy-induced resistance mechanism in glioblastoma

Project description:Analysis of mouse glioma tumors (in RAG1-/- mouse host) overexpressing Control(C) or Slug(S) viruses, and treated with doxycyclin(D) to turn off EGFRviii expression. Results provide insight into molecular basis of EGFRviii targeted therapy-induced resistence in GBM. By utilizing animals engineered with doxycycline (dox)-off oncogenic EGFRvIII transgene and conditional Ink4a/Arf and Pten alleles (Nestin-CreERT2; Ink4aL/L; PtenL/L; hGFAP_tTA; tetO-EGFRvIII, designated iEIP), we previously demonstrated that sustained oncogenic EGFR signaling was required for maintenance of EGFR-driven glioma progression and suppression of oncogenic EGFRvIII transgene expression induces tumor regression. But despite of a robust initial response, the regressed tumors relapsed inevitably. The finding that relapsed tumors had escaped oncogenic EGFR signaling addiction promoted our search for potential genetic events that might fuel the resistance development. Three relapse and two matched treatment-naïve tumors derived from the same parental line were analyzed by whole exome sequencing.

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