Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from TGF-beta-treated human ovarian fibroblasts

ABSTRACT: Advanced ovarian cancer is the most lethal gynecologic malignancy in the United States. Ovarian cancer cells are known to have diminished response to TGF-beta, but it remains unclear whether TGF-beta can modulate ovarian cancer cell growth in an indirect manner through cancer-associated fibroblasts (CAFs). Using transcriptome profiling analyses on TGF-beta-treated ovarian fibroblasts, we identified a TGF-beta-responsive gene signature in ovarian fibroblasts. Identifying TGF-beta-regulated genes in the ovarian microenvironment helps in understanding the role of TGF-beta in ovarian cancer progression. The human telomerase-immortalized ovarian fibroblast line NOF151 was treated with 5ng/mL of either TGF-beta-1 or TGF-beta-2. Total RNA was isolated from control samples and TGF-beta-treated fibroblasts samples at 48 hours post-treatment, followed by cDNA synthesis, IVT and biotin labeling. Samples were then hybridized onto Affymetrix Human Genome U133 Plus 2.0 microarrays. For each treatment group, three independent samples were prepared for the microarray experiment.

ORGANISM(S): Homo sapiens

SUBMITTER: Tsz-Lun Yeung

PROVIDER: E-GEOD-40266 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

TGF-β modulates ovarian cancer invasion by upregulating CAF-derived versican in the tumor microenvironment.

Yeung Tsz-Lun TL Leung Cecilia S CS Wong Kwong-Kwok KK Samimi Goli G Thompson Melissa S MS Liu Jinsong J Zaid Tarrik M TM Ghosh Sue S Birrer Michael J MJ Mok Samuel C SC

Cancer research 20130703 16

TGF-β has limited effects on ovarian cancer cells, but its contributions to ovarian tumor growth might be mediated through elements of the tumor microenvironment. In the present study, we tested the hypothesis that TGF modulates ovarian cancer progression by modulating the contribution of cancer-associated fibroblasts (CAF) that are present in the microenvironment. Transcriptome profiling of microdissected stromal and epithelial components of high-grade serous ovarian tumors and TGF-β-treated no ...[more]

PMID: 23824740

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Project description:Our group is interested in epithelial-to-mesenchymal transition (EMT), in particular, TGF-beta induced EMT. TGF-beta signalling has been shown to be an important factor in the induction of EMT and it has been demonstrated that adding TGF-beta to epithelial cells in culture is a convenient way to study the process of EMT. âIn response to TGF-beta, Smad2 and 3 are activated, and form complexes with Smad4, which then regulate transcription of target genes through interactions with other DNA binding transcription factors. In the induction of EMT, the activated Smads mediate transcriptional regulation through three families of transcription factors, resulting in repression of epithelial marker gene expression and activation of mesenchymal gene expressionâ (Xu J, et al. 2009) Also investigated in this study is the role of H2A.Z in EMT. H2A.Z is an evolutionary conserved and a metazoan essential histone variant of the H2A class. Mice deficient in H2A.Z die during early development but the reason for this is unknown (Faast et al. 2001). Previously, our laboratory showed that the loss of H2A.Z in Xenpous laevis impaired cell movement required for the formation of the mesoderm and neural crest (Ridgway et al. 2004). Given that mesoderm formation is critically dependent upon EMT, we therefore wondered whether H2A.Z might be a chromatin regulator of EMT. We transfected MDCK cells with a lentiviral vector to express a construct encoding an shRNA targeting canine H2A.Z as we wanted to test the hypothesis that H2A.Z is involved in the maintenance of cellular identity and that its loss might trigger de-differentiation. In order to investigate changes in gene expression associated with TGF-beta induced epithelial-to-mesenchymal transition (EMT) we performed paired end RNA-Seq of poly-A selected mRNA in untreated and TGFb-treated MDCK cells. The MDCK cell line has been extensively used as a model system for EMT because they convert fully from the epithelial to the mesenchymal state in response to TGF-beta. Gene expression profiles were also generated from MDCK cells in which H2A.Z was knocked down using shRNA. Please note that ChIP-seq data generated in conjunction to this RNA-seq data set were also deposited at ArrayExpress under accession number E-MTAB-5637 ( https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-5637 ).

Dataset Information

Expression data from TGF-beta-treated human ovarian fibroblasts

Publications

TGF-β modulates ovarian cancer invasion by upregulating CAF-derived versican in the tumor microenvironment.

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