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A PDGFRα-driven mouse model of Glioblastoma reveals a Stathmin1-mediated mechanism of sensitivity to Vinblastine

ABSTRACT: A PDGFRα-driven mouse model of Glioblastoma reveals a Stathmin1-mediated mechanism of sensitivity to Vinblastine

PROVIDER: PRJNA471344 | ENA |

REPOSITORIES: ENA

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A PDGFRα-driven mouse model of Glioblastoma reveals a Stathmin1-mediated mechanism of sensitivity to Vinblastine

Project description:Glioblastoma multiforme (GBM) is an aggressive primary brain cancer that includes focal amplification of PDGFRα and for which there are no effective therapies. Herein, we report the development of a genetically engineered mouse model of GBM based on autocrine, chronic stimulation of PDGFRα and the analysis of GBM signaling pathways using proteomics. We discovered the tubulin-binding protein Stathmin1 (STMN1) as a PDGFRα phospho-regulated target and that this mis-regulation conferred selective sensitivity to vinblastine (VB) cytotoxicity. Treatment of PDGFRα GBMs with VB in mice drastically prolonged survival and was dependent on STMN1. Our work provides a rationale for evaluating genotype-specific anti-microtubule drugs as cancer treatment in select GBM patient populations.

2018-05-15 | GSE114438 | GEO

PDGF-driven glioblastoma mouse model scRNA-Seq

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EGFR-targeted therapy-induced resistance mechanism in glioblastoma

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Expression data of PDGFRα- and PDGFRα+ mesenchymal stem cells isolated from mouse periosteum

Project description:Expression data of PDGFRα- and PDGFRα+ mesenchymal stem cells isolated from mouse periosteum

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Attenuating Hypoxia Driven Malignant Behavior in Glioblastoma with a Novel Hypoxia-Inducible Factor 2 Alpha Inhibitor

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Next Generation Sequencing Quantitative Analysis of altered expression of genes in BCa cells-induced PDGFRα+ITGA11+ CAFs and other CAFs

Project description:The cellular diversity of stromal compartment within the tumor microenvironment might change dynamically as tumors evolve that allowing distant dissemination of tumor cells and informing the treatment options. We used single cell RNA sequencing (scRNA-seq) to provide a detailed insight of cellular components feature in bladder cancer and identify that PDGFRα+ITGA11+ CAFs were essential for lymphatic metastasis of bladder cancer. To identify molecular mechanism of PDGFRα+ITGA11+ CAFs formation, next generation sequencing (NSG) was performed to explore the upregulated genes in bladder cancer-induced PDGFRα+ITGA11+ CAFs.

2024-02-16 | GSE252645 | GEO

An epigenetic mechanism underlying chromosome 17p deletion-driven tumorigenesis

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Intronic polyadenylation of PDGFRα in resident stem cells attenuates muscle fibrosis

Project description:The platelet-derived growth factor receptor alpha (PDGFRα) exhibits divergent effects in skeletal muscle. At physiological levels, signaling through this receptor promotes muscle development in growing embryos and proper angiogenesis in regenerating adult muscle. However, either increased PDGF ligands or enhanced PDGFRα pathway activity causes pathological fibrosis. This excessive collagen deposition, which is seen in aged and diseased muscle, interferes with proper muscle function and limits the effectiveness of gene- and cell-based therapies for muscle disorders. Although compelling evidence exists for the role of PDGFRα in fibrosis, little is known about the cells through which this pathway acts. Here we show that PDGFRα signaling regulates a population of muscle-resident fibro/adipogenic progenitors (FAPs) that play a supportive role in muscle regeneration but may also cause fibrosis when aberrantly regulated. We found that FAPs produce multiple transcriptional variants of PDGFRα with different polyadenylation sites, including an intronic variant that codes for a protein isoform containing a truncated kinase domain. This variant, upregulated during regeneration, acts as a decoy to inhibit PDGF signaling and to prevent FAP over-activation. Moreover, increasing expression of this isoform limits fibrosis in vivo, suggesting both biological relevance and therapeutic potential of modulating polyadenylation patterns in stem cell populations. We used microarrays to explore the biological effects of altering intronic polyadenylation of PDGFRα in FAPs.

2016-11-30 | GSE60099 | GEO

Intronic polyadenylation of PDGFRα in stromal stem cells attenuates muscle fibrosis

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PDGFRα+ not CD137+ progenitors control visceral obesity via glucocorticoid mediated TEAD1 methylation state

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