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Transcription profiling of glioblastoma primary culture treated with TGF-beta receptor inhibition.

ABSTRACT: TGF-beta has an oncogenic response in glioblastoma and it is considered to be a therapeutic target. We evaluated the effect of TGF-beta inhibition in glioblastoma. Differential gene expression analysis of patient-derived primary cultured glioblastoma cells treated with the TGF-beta receptor inhibitor, LY2109761 11 patient-derived cell cultures from 11 patients were treated with 2microM of the TGF-beta receptor inhibitor, LY2109761, for 3 hours or left untreated and RNA was isolated and microarray analysis was performed

ORGANISM(S): Homo sapiens

SUBMITTER: Joan Seoane

PROVIDER: E-GEOD-23935 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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TGF-β Receptor Inhibitors Target the CD44(high)/Id1(high) Glioma-Initiating Cell Population in Human Glioblastoma.

Anido Judit J Sáez-Borderías Andrea A Gonzàlez-Juncà Alba A Rodón Laura L Folch Gerard G Carmona Maria A MA Prieto-Sánchez Rosa M RM Barba Ignasi I Martínez-Sáez Elena E Prudkin Ludmila L Cuartas Isabel I Raventós Carolina C Martínez-Ricarte Francisco F Poca M Antonia MA García-Dorado David D Lahn Michael M MM Yingling Jonathan M JM Rodón Jordi J Sahuquillo Juan J Baselga José J Seoane Joan J

Cancer cell 20101201 6

Glioma-initiating cells (GICs), also called glioma stem cells, are responsible for tumor initiation, relapse, and therapeutic resistance. Here, we show that TGF-β inhibitors, currently under clinical development, target the GIC compartment in human glioblastoma (GBM) patients. Using patient-derived specimens, we have determined the gene responses to TGF-β inhibition, which include inhibitors of DNA-binding protein (Id)-1 and -3 transcription factors. We have identified a cell population enriched ...[more]

PMID: 21156287

Similar Datasets

Gene responses to TGF-beta receptor inhibition in glioblastoma

Project description:TGF-beta has an oncogenic response in glioblastoma and it is considered to be a therapeutic target. We evaluated the effect of TGF-beta inhibition in glioblastoma. Differential gene expression analysis of patient-derived primary cultured glioblastoma cells treated with the TGF-beta receptor inhibitor, LY2109761

2011-01-27 | GSE23935 | GEO

Glio-cellculture_Ly2109761

Project description:The effect of TGF-beta receptor inhibitor Ly2109761 on glioblastoma cells in combination with photon irradiation was analysed.

2011-08-27 | E-TABM-1148 | biostudies-arrayexpress

Transcription profiling of human glioma cells treated with TGF-beta or an inhibitor of the TGF-beta Receptor I LY2109761

Project description:In order to identify the genes that are regulated by TGF-beta in glioma, we serum starved two glioma cell lines, U373MG and U87MG, for 16h and we treated them with vehicle,100pM TGF-beta, 2uM inhibitor of the TGF-beta Receptor I(TbRI)(LY2109761), or both 100pM TGF-beta plus 2uM TbRI for 3h. Then, cell were collected and total RNA was extracted.

2007-05-16 | E-MEXP-903 | biostudies-arrayexpress

TGF-beta specific gene expression signatures in breast cancer stem cells

Project description:Analyze TGF-beta pathway transcriptional regulation in breast cancer stem cells with different responses upon TGF-beta pathway activation. Total RNA from four breast cell lines grown as mammospheres treated with recombinant TGF-beta or a TGF-beta receptor I inhibitor was used in the analysis.

2012-02-09 | E-MTAB-516 | biostudies-arrayexpress

Integration of TGF-β-induced Smad signaling in the insulin-induced transcriptional response in endothelial cells

Project description:The goal of the current study was to examine the extent to which TGF-beta signaling contributes to insulin-induced transcriptional responses in endothelial cells (HUVECs). HUVECs cells were treated with or without insulin in the absence or presence of SB431542, a TGF-beta receptor kinase inhibitor. Cells were sequenced using Hiseq 2000 (Illumina) as paired-end 2x100 base reads.

2019-10-30 | E-MTAB-8297 | biostudies-arrayexpress

Identification of TGF-β regulated lncRNAs in GBM cells using microarray screen

Project description:To identify TGF-β regulated lncRNAs in glioblastoma, we performed a genome-wide microarray screen in T98G glioma cells. T98G cells were treated with 10 ng/ml TGF-β (24h) and differentially expressed lncRNAs were identified using microarray in comparison with control cells.

2021-09-15 | GSE183211 | GEO

Vizan2013 - TGF pathway long term signaling

Project description:Pedro Vizán, Daniel S. J. Miller, Ilaria Gori, Debipriya Das, Bernhard Schmierer & Caroline S. Hill. Controlling long-term signaling: receptor dynamics determine attenuation and refractory behavior of the TGF-β pathway. Science Signaling 6, 305 (2013). Understanding the complex dynamics of growth factor signaling requires both mechanistic and kinetic information. Although signaling dynamics have been studied for pathways downstream of receptor tyrosine kinases and G protein (heterotrimeric guanine nucleotide-binding protein)-coupled receptors, they have not been investigated for the transforming growth factor-β (TGF-β) superfamily pathways. Using an integrative experimental and mathematical modeling approach, we dissected the dynamic behavior of the TGF-β to Smad pathway, which is mediated by type I and type II receptor serine/threonine kinases, in response to acute, chronic, and repeated ligand stimulations. TGF-β exposure produced a transient response that attenuated over time, resulting in desensitized cells that were refractory to further acute stimulation. This loss of signaling competence depended on ligand binding, but not on receptor activity, and was restored only after the ligand had been depleted. Furthermore, TGF-β binding triggered the rapid depletion of signaling-competent receptors from the cell surface, with the type I and type II receptors exhibiting different degradation and trafficking kinetics. A computational model of TGF-β signal transduction from the membrane to the nucleus that incorporates our experimental findings predicts that autocrine signaling, such as that associated with tumorigenesis, severely compromises the TGF-β response, which we confirmed experimentally. Thus, we have shown that the long-term signaling behavior of the TGF-β pathway is determined by receptor dynamics, does not require TGF-β-induced gene expression, and influences context-dependent responses in vivo.

2024-09-02 | BIOMD0000000499 | BioModels

TGF-beta-activated cancer-associated fibroblasts limit cetuximab efficacy in preclinical models of head and neck cancer

Project description:Most head and neck cancer (HNC) patients are resistant to cetuximab, an antibody against the epithelial growth factor receptor. Such therapy resistance is known to be mediated, in part, by stromal cells surrounding the tumor cells; however, the mechanisms underlying such a resistance phenotype remain unclear. To identify the mechanisms underlying cetuximab resistance in an unbiased manner, RNA-sequencing (RNA-seq) of HNC patient-derived xenografts (PDXs) was performed. Comparing the gene expression of HNC-PDXs before and after treatment with cetuximab indicated that the TGF-beta signaling pathway was upregulated in the stromal cells of PDXs that progressed to cetuximab (CetuximabProg-PDX). However, in PDXs that were extremely sensitive to cetuximab, and when tumors shrunk following cetuximab treatment (CetuximabSen-PDX), the TGF-beta pathway was downregulated in the stromal compartment. Histopathological analysis of PDXs showed that in CetuximabProg-PDX, TGF-beta-activation was detected in cancer-associated fibroblasts (CAFs). These TGF-beta-activated CAFs were sufficient to limit cetuximab efficacy in vitro and in vivo. Moreover, blocking the TGF-beta pathway using the SMAD3 inhibitor, SIS3, enhanced cetuximab efficacy and prevented the progression of CetuximabProg-PDX. Altogether, our findings indicate, for the first time, that TGF-beta-activated CAFs play a role in limiting cetuximab efficacy in HNC.

2020-03-23 | GSE143279 | GEO

Activation of TGF-beta pathway by areca nut constituents: A possible cause of Oral submucous fibrosis.

Project description:To understand the role of areca nut constituents in manifestation of Oral submucous fibrosis, we studied gene expression profile in epithelial cells following areca nut water extract treatment. A comaprison with TGF-beta induced gene expression changes were performed as epithelial cells were predicted to be source of TGF-beta. Control Vs Areca nut 5 ug/ml water extract (5H) (2), Contro Vs TGF-beta (2), Control Vs ALK5 (TbetaRI inhibitor) (2), Control Vs 5H + ALK5 inhibitor (2). (2)- Biological duplicates.

2013-05-22 | E-GEOD-38227 | biostudies-arrayexpress

Gene expression analysis of TGF-beta signaling-disrupting gastric cancer cell line 2MLN

Project description:Diffuse-type gastric carcinoma is a poor-prognostic cancer with high expression of transforming growth factor (TGF)-β and thick stromal fibrosis. However, detailed investigations on the roles of TGF-β signaling in diffuse-type gastric carcinoma have not been performed. We generated two diffuse-type gastric carcinoma cell lines, dominant-negative TGF-β type II receptor expressing cells (2MLN-dnTβRII) and GFP-expressing cells (2MLN-GFP). Cells were subcutaneously or orthotopically injected into nude mice. Although dnTβRII did not affect the growth of OCUM-2MLN in vitro, it accelerated the growth of subcutaneously or orthotopically transplanted tumors in vivo. By microarray analysis, we found gene expression of TSP-1, an angiogenic inhibitor, was down-regulated in dnTβRII tumors. This results suggested disruption of TGF-β signaling in diffuse-type gastric carcinoma cells leads to alteration of tumor microenvironment and acceleration of tumor growth. We generated two OCUM-2MLN-derived gastric carcinoma cell lines; 2MLN-dnTβRII, which expresses dominant negative form of TβRII, and control 2MLN-GFP, which expresses GFP. The transplanted tumors of these cell lines were subjected to gene expression analysis with Affymetrix U133 plus2 arrays.

2011-12-30 | E-GEOD-12336 | biostudies-arrayexpress

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