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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE77424 | GEO | 2016/03/22

SECONDARY ACCESSION(S): PRJNA310251

REPOSITORIES: GEO

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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 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.

2016-03-22 | E-GEOD-77419 | biostudies-arrayexpress

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.

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.

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

| PRJNA310251 | ENA

USP1 Promotes GC Metastasis via Stabilizing ID2.

Project description:Gastric cancer (GC) is one of the most common malignant tumors all over the world. And recurrence and metastasis are still the main causes of low survival rate for advanced GC. USP1 has been shown overexpressed in multiple cancers, which indicate its important biomarker in tumorigenesis and development. Our study is aimed at defining the exact role of USP1 on GC metastasis and the underlying mechanism. USP1 was firstly found overexpressed in GC tissues and relatively high-expression levels conferred poor survival rates. Then, real-time cellular analysis (RTCA) showed that USP1 knockdown inhibited GC metastasis both in vitro and in vivo. Mechanically, we demonstrated that USP1 promoted GC metastasis via upregulating ID2 expression and further confirmed that USP1 stabilized ID2 expression through deubiquitinating ID2 in GC. In conclusion, our study showed that USP1 promoted GC metastasis via stabilizing ID2 expression, which provides a potential biomarker and therapy target for GC.

| S-EPMC8643267 | biostudies-literature

TBK1 directly engages Akt/PKB survival signaling to support oncogenic transformation.

Project description:The innate immune-signaling kinase, TBK1, couples pathogen surveillance to induction of host defense mechanisms. Pathological activation of TBK1 in cancer can overcome programmed cell death cues, enabling cells to survive oncogenic stress. The mechanistic basis of TBK1 prosurvival signaling, however, has been enigmatic. Here, we show that TBK1 directly activates AKT by phosphorylation of the canonical activation loop and hydrophobic motif sites independently of PDK1 and mTORC2. Upon mitogen stimulation, triggering of the innate immune response, re-exposure to glucose, or oncogene activation, TBK1 is recruited to the exocyst, where it activates AKT. In cells lacking TBK1, insulin activates AKT normally, but AKT activation by exocyst-dependent mechanisms is impaired. Discovery and characterization of a 6-aminopyrazolopyrimidine derivative, as a selective low-nanomolar TBK1 inhibitor, indicates that this regulatory arm can be pharmacologically perturbed independently of canonical PI3K/PDK1 signaling. Thus, AKT is a direct TBK1 substrate that connects TBK1 to prosurvival signaling.

| S-EPMC3073833 | biostudies-literature

A recombinant lentiviral PDGF-driven mouse model of proneural glioblastoma.

Project description:Background:Mouse models of glioblastoma (GBM), the most aggressive primary brain tumor, are critical for understanding GBM pathology and can contribute to the preclinical evaluation of therapeutic agents. Platelet-derived growth factor (PDGF) signaling has been implicated in the development and pathogenesis of GBM, specifically the proneural subtype. Although multiple mouse models of PDGF-driven glioma have been described, they require transgenic mice engineered to activate PDGF signaling and/or impair tumor suppressor genes and typically represent lower-grade glioma. Methods:We designed recombinant lentiviruses expressing both PDGFB and a short hairpin RNA targeting Cdkn2a to induce gliomagenesis following stereotactic injection into the dentate gyrus of adult immunocompetent mice. We engineered these viruses to coexpress CreERT2 with PDGFB, allowing for deletion of floxed genes specifically in transduced cells, and designed another version of this recombinant lentivirus in which enhanced green fluorescent protein was coexpressed with PDGFB and CreERT2 to visualize transduced cells. Results:The dentate gyrus of injected mice showed hypercellularity one week post-injection and subsequently developed bona fide tumors with the pathologic hallmarks of GBM leading to a median survival of 77 days post-injection. Transcriptomic analysis of these tumors revealed a proneural gene expression signature. Conclusion:Informed by the genetic alterations observed in human GBM, we engineered a novel mouse model of proneural GBM. While reflecting many of the advantages of transgenic mice, this model allows for the facile in vivo testing of gene function in tumor cells and makes possible the rapid production of large numbers of immunocompetent tumor-bearing mice for preclinical testing of therapeutics.

| S-EPMC5817944 | biostudies-literature

Genetic variants of PDGF signaling pathway genes predict cutaneous melanoma survival.

Project description:To investigate whether genetic variants of platelet-derived growth factor (PDGF) signaling pathway genes are associated with survival of cutaneous melanoma (CM) patients, we assessed associations of single-nucleotide polymorphisms in PDGF pathway with melanoma-specific survival in 858 CM patients of M.D. Anderson Cancer Center (MDACC). Additional data of 409 cases from Harvard University were also included for further analysis. We identified 13 SNPs in four genes (COL6A3, NCK2, COL5A1 and PRKCD) with a nominal P < 0.05 and false discovery rate (FDR) < 0.2 in MDACC dataset. Based on linkage disequilibrium, functional prediction and minor allele frequency, a representative SNP in each gene was selected. In the meta-analysis using MDACC and Harvard datasets, there were two SNPs associated with poor survival of CM patients: rs6707820 C>T in NCK2 (HR = 1.87, 95% CI = 1.35-2.59, Pmeta= 1.53E-5); and rs2306574 T>C in PRKCD (HR = 1.73, 95% CI = 1.33-2.24, Pmeta= 4.56E-6). Moreover, CM patients in MDACC with combined risk genotypes of these two loci had markedly poorer survival (HR = 2.47, 95% CI = 1.58-3.84, P < 0.001). Genetic variants of rs6707820 C>T in NCK2 and rs2306574 T>C in PRKCD of the PDGF signaling pathway may be biomarkers for melanoma survival.

| S-EPMC5650365 | biostudies-literature

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