Project description:siSTAT3 knockdown of a tamoxifen initiated, transformation inducible, breast cancer model system (MCF10A-ER-Src), with associated controls of EtOH and siNEG treatments. A description of MCF10A-ER-Src cells can be found here: www.encodeproject.org
Project description:ChIP-Seq was performed on naiive cell lines from a Breast Cancer Progression model, including MCF10A, MCF10AT1, and DCIS. Biological replicates (n=2) were performed for all factors across all cell lines described.
Project description:With this experiment, we aimed to decipher the epigenetic changes occuring during tumour progression in a model of basal-like breast cancer, based on immortalized mammary epithelial cells (IMEC). The tumorigenic IMEC, xenograft-derived and metastasis-derived cells were used for the analysis
Project description:With this experiment, we aimed to decipher the changes in chromatin accessibility during tumour progression in a model of basal-like breast cancer, based on immortalized mammary epithelial cells (IMEC). The tumorigenic IMEC, xenograft-derived and metastasis-derived cells were used for the analysis
Project description:The non-tumourigenic human breast epithelial cell line MCF10A is the cell line most commonly used as a model for normal human breast cells. This dataset provides a reference genome for MCF10A. The whole genome, high-throughput sequencing was performed using the Illumina NovaSeq 6000 PE150 system. Both NGS and bioinformatic analysis were performed by Novogene (UK).
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.
Project description:The molecular signature at histone H3K4 involved in epigenetic regulation of normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology. This study examines the dynamic distribution of H3K4me3 and H3K4ac histone modification associated with active chromatin to provide an understanding of the changes in epigenetic regulation associated with the unique breast cancer subtypes. H3K4me3 and H3K4ac histone modification study in normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology
Project description:The epigenetic influence from microenvironment on mammary epethelial cells was investigated by coculture MCF10A cells with different breast fibroblasts that extracted from either breast cancer tissues or normal breast tissues. Experiment Overall Design: MCF10A cells were cocultured with different breast fibroblasts that extracted from either breast cancer tissues or normal breast tissues. After three weeks coculture, MCF10A cells were sorted and harvested for total RNA extraction. Affymetrix expression microarray was performed to analyse gene expression changes.
