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PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-mediated Survival of Proneural Glioma Cells.

ABSTRACT: Identification of critical survival determinants of PDGF-driven proneural glioma. Results provided information about the genes and pathways that are regulated by PDGF signaling in PDGF-driven proneural glioma and led to the assessment of the importance of the USP1-ID2 axis in proneural glioma. Total RNA was obtained from untreated and Dox treated PDGF-driven glioma spheroid cells (PDGF-GSC) which had been isolated from the Gfap-tTa/Tre-PDGFB mouse model used in our study. The data were analyzed to determine the genes that are regulated by PDGF signaling in PDGF-driven glioma.

ORGANISM(S): Mus musculus

SUBMITTER: Gilbert Rahme

PROVIDER: E-GEOD-77419 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-Mediated Survival of Proneural Glioma Cells.

Rahme Gilbert J GJ Zhang Zhonghua Z Young Alison L AL Cheng Chao C Bivona Eric J EJ Fiering Steven N SN Hitoshi Yasuyuki Y Israel Mark A MA

Cancer research 20160307 10

Glioblastoma is the most aggressive primary brain tumor and responds poorly to currently available therapies. Transcriptomic characterization of glioblastoma has identified distinct molecular subtypes of glioblastoma. Gain-of-function alterations leading to enhanced platelet-derived growth factor (PDGF) signaling are commonly observed in the proneural subtype of glioblastoma and can drive gliomagenesis. However, little is known about the downstream effectors of PDGF signaling in glioblastoma. Us ...[more]

PMID: 26951930

Similar Datasets

PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-mediated Survival of Proneural Glioma Cells.

Project description:Identification of critical survival determinants of PDGF-driven proneural glioma. Results provided information about the genes and pathways that are regulated by PDGF signaling in PDGF-driven proneural glioma and led to the assessment of the importance of the USP1-ID2 axis in proneural glioma. Total RNA obtained from PDGF-driven glioma spheroid cells (PDGF-GSC) and primary tumors arising in the Gfap-tTa/Tre-PDGFB mouse model used in our study was analyzed to determine to which subtype of GBM these specimens belonged.

2016-03-22 | E-GEOD-77423 | biostudies-arrayexpress

PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-mediated Survival of Proneural Glioma Cells.

2016-03-22 | GSE77423 | GEO

PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-mediated Survival of Proneural Glioma Cells.

2016-03-22 | GSE77419 | GEO

PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-mediated Survival of Proneural Glioma Cells.

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-03-22 | E-GEOD-77424 | biostudies-arrayexpress

PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-mediated Survival of Proneural Glioma Cells.

Project description:PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-mediated Survival of Proneural Glioma Cells.

| PRJNA310251 | ENA

Clemastine suppresses proneural glioblastoma stem cell growth

Project description:Glioblastoma (GBM) cells’ stemness-like features and lineage plasticity promote tumor progression. Here, we demonstrate that Clemastine, a drug for treating hay fever and allergy symptoms, effectively attenuated the stemness and suppressed the propagation of primary GBM cultures bearing PDGFRA amplification. We show that these effects of GBM cells were accompanied by altered gene expression profiling indicative of a more differentiated state of tumor cells, in resonating with Clemastine’s activity in promoting the differentiation of normal oligodendrocyte progenitors (OPCs) into mature oligodendrocyte. Functional assays for proteins that can be pharmacologically targeted by Clemastine, including histamine receptors, muscarinic receptors, and Emopamil binding protein (EBP), revealed the essential roles of these proteins in sustaining GBM cell propagation and suggested that Clemastine likely impairs tumor cells via targeting multiple pathways. Finally, we showed that a PDGFB-driven mouse glioma model, representing the proneural subtype GBMs, was similarly susceptible to Clemastine treatment. Collectively, these results identify pathways that are essential for maintaining the proneural progenitor features of GBMs, and suggest that non-oncology, low toxicity drugs with OPC differentiation promoting effects, such as Clemastine, can be exploited for targeting GBM cell’s progenitor property.

2023-10-04 | GSE186319 | GEO

Clemastine suppresses proneural glioblastoma stem cell growth II

2023-10-04 | GSE186392 | GEO

Prominin 1/CD133 Endothelium Sustains Growth of Proneural Glioma

Project description:As many other tumors, a subset of gliobastoma is thought to be maintained by a restricted population of cancer cells, stem-like cells that express CD133 transmembrane protein. Expression levels of CD133 gene has been linked to a poor prognostic molecular subgroup and is not overexpressed by the PDGF-driven proneural group. Thus, the significance of CD133+ cells for gliomagenesis of the proneural group is undetermined. In addition, the role of the CD133 protein remains elusive and controversial, which results from the difficult isolation of CD133+ cells that has largely relied on the use of antibodies to ill-defined glycosylated epitopes of CD133. Here, we used a knockin lacZ reporter mouse, Prom1lacZ/+, to track Prom1+ cells in the brain and found that Prom1 (prominin1, murine CD133 homologue) is expressed by cells that co-express markers characteristic of neuronal, glial and vascular lineage phenotype. In proneural tumors derived from injection of RCAS-PDGF into the brain of tv-a;Ink4a-Arf-/- Prom1lacZ/+ mice, Prom1+ cells co-express markers for astrocytes and endothelial cells. Therefore, we characterize the tumor propagation in a murine model and found that the mice co-transplanted with Prom1 endothelium and proneural tumor spheres cells had significant tumor burden and vascular proliferation (angiogenesis). Specific genes in Prom1 endothelium are identified that code for endothelial signaling modulators that most likely support proneural tumor progression and can be potential targets for anti-angiogenic therapy. Cells were sorted via FACS to obtain a population of CD31+CD133- cells and a population of CD31+CD133+ cells. Total RNA was extracted from each population and gene expression was assayed on Affymetrix Mouse 430 2.0 arrays with one array per cell population.

2013-12-31 | E-GEOD-43931 | biostudies-arrayexpress

Prominin 1/CD133 Endothelium Sustains Growth of Proneural Glioma

2013-12-31 | GSE43931 | GEO

Glioblastoma Genetic Drivers Dictate the Function of Tumor-Associated Macrophages/Microglia and Responses to CSF1R Inhibition

Project description:Tumor-associated macrophages/microglia (TAMs) are prominent microenvironment components in human glioblastoma (GBM) that are potential targets for anti-tumor therapy. However, TAM depletion by CSF1R inhibition showed mixed results in clinical trials. We hypothesized that GBM subtype-specific tumor microenvironment convey distinct sensitivities to TAM targeting.We generated syngeneic PDGFB-driven and RAS-driven GBM models that resemble proneural-like and mesenchymal-like gliomas, and determined the effect of TAM targeting by CSF1R inhibitor PLX3397 on glioma growth. We also investigated the co-targeting of TAMs and angiogenesis on PLX3397-resistant RAS-driven GBM. Using single-cell transcriptomic profiling, we further explored differences in tumor microenvironment cellular compositions and functions in PDGFB- and RAS-driven gliomas. We found that growth of PDGFB-driven tumors was markedly inhibited by PLX3397. In contrast, depletion of TAMs at the early phase accelerated RAS-driven tumor growth and had no effects on other proneural and mesenchymal GBM models. In addition, PLX3397-resistant RAS-driven tumors did not respond to PI3K signaling inhibition. Single-cell transcriptomic profiling revealed that PDGFB-driven gliomas induced expansion and activation of pro-tumor microglia, whereas TAMs in mesenchymal RAS-driven GBM were enriched in pro-inflammatory and angiogenic signaling. Co-targeting of TAMs and angiogenesis decreased cell proliferation and changed the morphology of RAS-driven gliomas.Our work identify functionally distinct TAM subpopulations in the growth of different glioma subtypes. Notably, we uncover a potential responsiveness of resistant mesenchymal-like gliomas to combined anti-angiogenic therapy and CSF1R inhibition. These data highlight the importance of characterization of the microenvironment landscape in order to optimally stratify patients for TAM-targeted therapy.

2021-10-08 | GSE185420 | GEO

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