Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA156523 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:TGF-betas have complex roles in tumorigenesis, with context-dependent effects that can either suppress or promote tumor progression. We have previously shown that TGF-beta has tumor suppressor activity in the MCF10Ca1h (M3) human breast cancer xenograft model. To identify potential molecular players in the tumor suppressor responses, we performed global gene expression analyses. To determine which genes were regulated by TGF-beta in this tumor model in vivo, we performed gene expression arrays on tumors derived from xenografts of M3 cells with and without expression of a dominant negative TGF-beta receptor to block activity of endogenous TGF-beta.
2015-01-01 | GSE34276 | 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: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:Profiling of TGF-beta regulated genes in immortal and tumor cell-lines
| PRJNA173466 | ENA
Project description:Inappropriate activation of developmental pathways is a well-recognized tumor-promoting mechanism. Here we show that overexpression of the homeoprotein Six1, normally a developmentally restricted transcriptional regulator, increases Transforming Growth Factor-beta (TGF-beta) signaling in mammary carcinoma cells and induces an epithelial to mesenchymal transition (EMT) that is in part dependent on its ability to increase TGF-beta signaling. TGF-beta signaling and EMT have been implicated in metastatic dissemination of carcinoma. Using spontaneous and experimental metastasis mouse models, we demonstrate that Six1 overexpression promotes breast cancer metastasis. In addition, we show that, like its induction of EMT, Six1-induced experimental metastasis is dependent on its ability to activate TGF-beta signaling. Importantly, in human breast cancers Six1 significantly correlates with nuclear Smad3, and thus increased TGF-beta signaling. Further, breast cancer patients whose tumors overexpress Six1 have a shortened time to relapse and metastasis, and an overall decrease in survival. Finally, we show that the effects of Six1 on tumor progression likely extend beyond breast cancer, since its overexpression correlates with adverse outcomes in numerous other cancers, including brain, cervical, prostate, colon, kidney, and liver, amongst others. Our findings argue that Six1, acting through TGF-beta signaling and EMT, is a powerful and global promoter of cancer metastasis.
2010-08-21 | GSE23655 | GEO
Project description:To understand the molecular mechanism of action of TGF-beta as a tumor suppressor in breast cancer. Comparison of gene expression between MCF10ACa1h breast tumor xenograft with or without an intact TGF-beta response. Keywords: genetic modification design
2007-06-01 | GSE5265 | GEO
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:The study aims: 1-to identify transcripts that are regulated during breast tumor cell plasticity induced by TGF-beta or by the silencing of PCBP1 expression and 2- to analyze the function of Platr18 lincRNA in breast cancer cells transcriptome reprogramming.
2021-10-20 | GSE146273 | GEO