Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA173466 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The study was carried out to delineate distinct TGF-beta target genes in immortal fibroblasts (HFhTERT), transformed fibroblasts (hFhTERT-LTgRAS) and tumor cells (HT1080). The data would help us in understanding the dual nature of TGF-beta.
2015-03-16 | GSE40315 | GEO
Project description:TGF-betas have complex roles in tumorigenesis, with context-dependent effects that can either suppress or promote tumor progression. Our goal was to use integrated genomic approaches in a model of human breast cancer progression to identify core TGF-beta-regulated genes that specifically reflect the tumor suppressor activity of TGF-beta. The model consisted of the non-tumorigenic MCF10A (“M1”), the premalignant MCF10AT1k.cl2 (“M2”), the early malignant MCF10Ca1h (“M3”) and the highly malignant, metastatic MCF10Ca1a.cl1 (“M4”) cell lines. We have previously shown that tumor suppressor activity of TGF-beta is lost in the highly malignant M4 cells. To determine how the spectrum of TGF-beta-regulated genes changes with cancer progression, we performed gene expression array analysis on four cell lines of the MCF10A-based model of breast cancer progression (M1-M4) cultured in vitro under serum-free conditions and treated with TGF-beta (5ng/ml plus condition) or vehicle (minus condition) for 1h or 6h.
2015-01-01 | GSE34270 | GEO
Project description:TGF-betas have complex roles in tumorigenesis, with context-dependent effects that can either suppress or promote tumor progression. Our goal was to use integrated genomic approaches in a model of human breast cancer progression to identify core TGF-beta-regulated genes that specifically reflect the tumor suppressor activity of TGF-beta. The model consisted of the non-tumorigenic MCF10A (“M1”), the premalignant MCF10AT1k.cl2 (“M2”), the early malignant MCF10Ca1h (“M3”) and the highly malignant, metastatic MCF10Ca1a.cl1 (“M4”) cell lines. We have previously shown that tumor suppressor activity of TGF-beta is dependent on Smad3, and is lost in M4 cells. To identify how TGF-beta/Smad3 targets change with cancer progression, we performed promoter-wide Smad3 ChIP-chip on all four cell lines of the breast cancer progression model (M1-M4), following treatment with TGF-beta or vehicle control.
2015-01-01 | GSE34271 | GEO
Project description:TGF-beta signature in cholangiocarcinoma cell lines
| PRJNA396687 | ENA
Project description:In this project we evaluated the proteomic profiling with TGF-β stimuli at 24h in a CRISPR-Cas9 model for ALMS1 gene in hTERT-BJ-5ta cells. Proteomic results showed a majority inhibition of downstream regulated pathways by the TGF-β, associating the protein coding genes (PCG) with processes like TGF- β matrix regulation, epithelial mesenchymal transition (EMT), PI3K/AKT or P53. In conclusion, seems that the depletion of ALMS1 could be inhibiting the signals transduction through the TGF -β and the routes regulated downstream.
2024-01-26 | PXD035708 | Pride
Project description:Profiling of genes regulated by TGF-beta in immortalized skin keratinocyte cells(HaCaT).
| PRJNA99761 | ENA
Project description:In this project we evaluated the proteomic profiling with TGF-β stimuli at 24h in a CRISPR-Cas9 model for ALMS1 gene in HeLa cells. Proteomic results showed a majority inhibition of downstream regulated pathways by the TGF-β, associating the protein coding genes (PCG) with processes like focal adhesion or cell-substrate adherens junction. Finally, EMT biomarkers like VIM, DSP, EDIL3 and SNAI1 had the opposite pattern to what would be expected when activating the EMT. In conclusion, seems that the depletion of ALMS1 could be inhibiting the signals transduction through the TGF -β and the routes regulated downstream by it such as the EMT.
2023-03-11 | PXD024964 | Pride
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
Project description:TGF-β signaling and its induced EMT (Epithelial to mesenchymal transition) play fundamental roles in development and disease including cancers. Although, TGF-β-regulated genes have been extensively studied, with RNA-sequencing (RNA-seq) analysis, new TGF-β-regulated genes are still been identified. Moreover, many significantly regulated genes by TGF-β are not emphasized. This study employs RNA-seq on MCF10A cells treated by TGF-β for 1.5 (this GEO), 24, 48, and 72 (GSE74377) hours and aims to identify novel TGF-β-regulated genes. With 1.5 fold gene expression change (log2 0.58) and p<0.05 at any length of the treatment, 1166 and 861 genes were found to be upregulated and downregulated by TGF-β, respectively. These genes were analyzed for their enrichments in KEGG pathways and prognostic markers of cancers. Several genes of interest were further analyzed for their regulation by TGF-β across cell lines and their functions in context of TGF-β were further studied. This study systematically analyzed TGF-β-regulated genes and revealed novel factors mediating the pro-migratory role of TGF-β signaling, hence, sheds a light on the understanding of the mechanisms underlying the role of TGF-β signaling in cancer development.
2019-01-18 | GSE125280 | GEO
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