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CCDC50 promotes glioblastoma progression through regulating EGFR cell-surface recycle

ABSTRACT: CCDC50 promotes glioblastoma progression through regulating EGFR cell-surface recycle

PROVIDER: PRJNA1004099 | ENA |

REPOSITORIES: ENA

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CCDC50 promotes glioblastoma progression through regulating EGFR cell-surface recycle

Project description:Glioblastomas (GBM) are a kind of malignant tumor with high mortality. However, the mechanism of tumor progression remains poorly understood. Specifically, we find that the expression of autolysosome-associated protein CCDC50, is positively correlated with tumor malignancy, and poor survival of GBM patients. CCDC50 functions as a specific cargo adaptor to assist EGFR recycling back to the plasma membrane, leading to prolonged activation of the downstream signaling pathways. We reveal that targeting CCDC50 in GBM may be a promising therapeutic strategy, as CCDC50 deficiency significantly inhibited the proliferation and migration of tumor cells in vitro and in vivo. Moreover, targeting CCDC50 together with alkylating agent temozolomide (TMZ) induces synergistic function in regression of GBM tumors, representing an alternative strategy for malignant tumor therapy. We performed transcriptome profiling (RNA-seq) and quantitative reverse transcription polymerase chain reaction (qRT–PCR) in shCtrl and shCCDC50 cells to evaluate the GBM tumor growth and metastasis controlled by CCDC50.

2023-08-21 | GSE240516 | GEO

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.

2023-01-25 | GSE222515 | GEO

Chromosome topology of the EGFR locus in glioblastoma

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).

2019-11-25 | GSE139414 | GEO

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.

2015-09-14 | E-GEOD-72468 | biostudies-arrayexpress

EGFR and EGFRvIII coopt host defense pathways, promoting progression in glioblastoma

Project description:To investigate the function of TLR2 in EGFR and EGFRvIII co-expressing glioblastoma cells, we knocked out TLR2 by CRISPR.

2024-08-29 | GSE212325 | GEO

Chromosome topology of the EGFR locus in glioblastoma

Project description:Chromosome topology of the EGFR locus in glioblastoma

| PRJNA579586 | ENA

EGFR-targeted therapy-induced resistance mechanism in glioblastoma

Project description:EGFR-targeted therapy-induced resistance mechanism in glioblastoma

| PRJNA428218 | ENA

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

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

| PRJNA1060727 | ENA

EGFR Mutation Promotes Glioblastoma Through Epigenome and Transcription Factor Network Remodeling

2015-09-14 | GSE72468 | GEO

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.

2022-07-01 | GSE183910 | GEO

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