Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA96371 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:ZEB1 binding sites in TGF-beta-stimulated MCF7 breast cancer cell line
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Project description:SIRT7 Antagonizes TGF-β Signaling and Inhibits Breast Cancer Metastasis
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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
Project description:Transforming growth factor-β (TGF-β) comprises a key component in the tumor microenvironment. It is reported that TGF-β can be pro-tumorigenic or anti-tumorigenic depending on various contexts. Some of the triple negative breast cancers highly express TGF-β, but pro-tumorigenic function of TGF-β in triple negative breast cancer cells is not fully known. Therefore, we analyzed genome-wide gene expression changes after stimulation with TGF-β in a triple negative breast cancer cell line, Hs578T cells.
2020-12-24 | GSE152414 | 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:Cancer Associated Fibroblasts (CAF) are a dominant and critical cell type of the tumour microenvironment and can lead to breast cancer progression. TGF-β has been reported to influence fibroblast to myofibroblast activation, which is similar to cancer associated fibroblast phenotype. To understand the mechanism of TGF-β mediated CAF phenotype, we have performed a comparative proteomic analysis of conditioned media from CAF (isolated from breast cancer biopsy tissues) and normal mammary fibroblasts engineered to over-express TGF-β1. Liquid chromatography/ tandem mass spectrometry (LC ESI Q-TOF-MS/MS) assay of conditioned media and Venn analysis of the acquired data, revealed approximately 185 common proteins secreted by the three fibroblast types (CAF, normal mammary fibroblasts and TGF-β over expressing mammary fibroblasts). Among these, 12 proteins exclusively overlap between normal fibroblasts and CAF and 20 proteins exclusively overlap between CAF and TGF-β1 over-expressing fibroblasts. This analysis reveals interesting targets which may be important in activation phenotype of CAF and breast cancer progression.
2025-08-26 | PXD022374 | Pride
Project description:TGF-beta signature in cholangiocarcinoma cell lines
| PRJNA396687 | ENA
Project description:RATIONALE: Measuring levels of transforming growth factor-beta (TGF-beta) in the blood of patients with epithelial cancers (head and neck, lung, breast, colorectal, and prostate) may help doctors predict how patients will respond to treatment with radiation therapy.
PURPOSE: This research study is measuring levels of TGF-beta in patients with epithelial cancers who are undergoing radiation therapy.
| 2072028 | ecrin-mdr-crc
Project description:Transforming growth factor (TGF)-β signaling enhances cancer cell plasticity by inducing epithelial-to-mesenchymal transition (EMT). Here, we identified a TGF-β-induced long non-coding RNA (lncRNA) LIMD1 Antisense RNA 1 (LIMD1-AS1) that strengthens the SMAD-mediated transcriptional response to TGF-β. The expression of LIMD1-AS1 is upregulated in breast cancer tissues compared to that of normal breast tissues, and high LIMD1-AS1 expression is associated with poor prognosis in breast cancer patients. Depletion of LIMD1-AS1 hinders TGF-β-induced EMT, migration, and extravasation of breast cancer cells. Mechanistically, LIMD1-AS1 promotes the interaction between SMAD3 and its transcriptional coactivator p300, and thereby enhances SMAD3 transcriptional activity and TGF-β/SMAD signaling. We showed that LIMD1-AS1 binds to the MAD homology 2 (MH2) domain of SMAD3 and the interferon-binding domain (IBiD) of p300. Displacing the binding of LIMD1-AS1 to p300 with its competitor interferon regulatory factor 3 (IRF3) suppressed the effects of LIMD1-AS1 on potentiating TGF-β/SMAD signaling. Moreover, blockage of p300 acetyltransferase activity with a pharmacological inhibitor, A-485, reduces the ability of LIMD1-AS1 to enhance SMAD3 transcriptional activity, TGF-β-induced EMT, and migration. This study reveals LIMD1-AS1 as a novel stimulator of TGF-β signaling by establishing a positive feedback loop and highlights its potential as a therapeutic target for breast cancer.
2025-07-08 | GSE288909 | GEO