Similar Datasets
Project description:We performed small RNA sequencing of conditioned media collected from breast cancer cells as well as human mammary epithelial cells (HUMEC) in biological replicates.
2018-11-05 | GSE114327 | GEO
Project description:We performed small RNA sequencing of exosomes and extracellular vesicles collected from breast cancer cells as well as human mammary epithelial cells (HUMEC) in biological replicates (using Norgen's cell culture media exosme purification and RNA isoaltion kits).
2018-11-05 | GSE114329 | GEO
Project description:The goal of this experiment was to identify genes that were expressed at higher levels in benign human mammary epithelial cells than in breast cancer cell lines and that were induced by 5AZA treatment in breast cancer cell lines. Six breast cancer cell lines were selected for demethylation studies based on known tumor suppressor gene expression regulation by promoter region hypermethylation: HCC1569 (CCND2), HCC1954 (SCGB3A1, APC, RASSF1A), MCF-7 (RAR-beta2), MDA-MB-231 (ESR1), UACC3199 (BRCA1), and BT-549 (hypermethylator phenotype). Other than MCF10A we specifically avoided immortalized benign human mammary epithelial cell lines for this experiment as these cells frequently show tumor suppressor gene methylation (e.g. p16) and gene expression profiles that are intermediate between normal breast epithelial cells and breast cancer. Instead, we opted to test six first-passage benign human mammary epithelial cell cultures (HME) generated in serum-free media from small fragments of normal breast tissue obtained from young women undergoing fibroadenoma excision. The 5AZA dose (0.5 microM) was selected based on evaluation of growth curves and induction of BNC1, SERPINB, and TKTL1 gene expression measured by RT-PCR in benign and malignant cells. The breast cancer cell lines, HME cultures, and MC10A cells were treated with 0.5 microM 5AZA (Sigma-Aldrich, St. Louis, MO) in DMSO or DMSO alone for six days after which the cells were harvested, and RNA prepared using the Illumina TotalPrep kit (AMIL1791, Life Technologies, Grand Island, NY). Whole genome expression was assessed using the Illumina HumanWG-6-v3 chip Gene expression was evaluated in 6 breast cancer cell lines, 6 primary breast epithelial cell cultures, and MCF10A cells after 6 days in DMSO or DMSO plus 0.5 microM 5AZA.
2012-10-19 | E-GEOD-41692 | biostudies-arrayexpress
Project description:The expression levels of tRNA-derived small RNA, known as tsRNA, were interrogated in the following parental cell lines: MCF10A normal-like mammary epithelial cell, MCF7, MCF10AT1, MCF10CA1a, and MDA-MB-231 breast cancer cells. In addition, tsRNA expression was determined after shRNA-inhibition of RUNX1 in MCF10A cells or RUNX1 induction in MCF10CA1a cells.
2020-01-01 | GSE142382 | GEO
Project description:The goal of this experiment was to identify genes that were expressed at higher levels in benign human mammary epithelial cells than in breast cancer cell lines and that were induced by 5AZA treatment in breast cancer cell lines. Six breast cancer cell lines were selected for demethylation studies based on known tumor suppressor gene expression regulation by promoter region hypermethylation: HCC1569 (CCND2), HCC1954 (SCGB3A1, APC, RASSF1A), MCF-7 (RAR-beta2), MDA-MB-231 (ESR1), UACC3199 (BRCA1), and BT-549 (hypermethylator phenotype). Other than MCF10A we specifically avoided immortalized benign human mammary epithelial cell lines for this experiment as these cells frequently show tumor suppressor gene methylation (e.g. p16) and gene expression profiles that are intermediate between normal breast epithelial cells and breast cancer. Instead, we opted to test six first-passage benign human mammary epithelial cell cultures (HME) generated in serum-free media from small fragments of normal breast tissue obtained from young women undergoing fibroadenoma excision. The 5AZA dose (0.5 microM) was selected based on evaluation of growth curves and induction of BNC1, SERPINB, and TKTL1 gene expression measured by RT-PCR in benign and malignant cells. The breast cancer cell lines, HME cultures, and MC10A cells were treated with 0.5 microM 5AZA (Sigma-Aldrich, St. Louis, MO) in DMSO or DMSO alone for six days after which the cells were harvested, and RNA prepared using the Illumina TotalPrep kit (AMIL1791, Life Technologies, Grand Island, NY). Whole genome expression was assessed using the Illumina HumanWG-6-v3 chip
2012-10-19 | GSE41692 | GEO
Project description:Background: Higher-order chromatin structure is often perturbed in cancer and other pathological states. Although several genetic and epigenetic differences have been charted between normal and breast cancer tissues, changes in higher-order chromatin organization during tumorigenesis have not been fully explored. To probe the differences in higher-order chromatin structure between mammary epithelial and breast cancer cells, we performed Hi-C analysis on MCF-10A mammary epithelial and MCF-7 breast cancer cell lines. Results: Our studies reveal that the small, gene-rich chromosomes chr16 through chr22 in the MCF-7 breast cancer genome display decreased interaction frequency with each other compared to the inter-chromosomal interaction frequency in the MCF-10A epithelial cells. Interestingly, this finding is associated with a higher occurrence of open compartments on chr16-22 in MCF-7 cells. Pathway analysis of the MCF-7 up-regulated genes located in altered compartment regions on chr16-22 reveals pathways related to repression of WNT signalling. There are also differences in intra-chromosomal interactions between the cell lines; telomeric and sub-telomeric regions in the MCF-10A cells display more frequent interactions than are observed in the MCF-7 cells. Conclusions: We show evidence of an intricate relationship between chromosomal organization and gene expression between epithelial and breast cancer cells. Importantly, this work provides a genome-wide view of higher-order chromatin dynamics and a resource for studying higher-order chromatin interactions in two cell lines commonly used to study the progression of breast cancer. Hi-C experiments were conducted in MCF-7 and MCF-10A parental cells. The RNA-seq data associated with this study is deposited under the GEO accession number GSE71862.
2015-09-02 | E-GEOD-66733 | biostudies-arrayexpress
Project description:Purpose: Gene expression analysis of knockdown and overexpression of LBH (Limb-Bud-and-Heart) in human breast cancer cell lines using RNA-Seq Methods: RNA was collected and analyzed from three biological replicates of each condition (LBH vs vector) for LBH overexpression (OE) in two human breast cancer cell lines (BT549, MCF7). Additionally, RNA was collected and analyzed from three biological replicates of each condition (siLBH vs non-target/NT siRNA) for LBH knockdown (KD) in two human triple negative breast cancer cells lines (HCC1395, MDA-MB-231). High-throughput sequencing used Illumina platforms. Results: Using an optimized data analysis workflow, we mapped about 60 million sequence reads per sample to the human genome (build hg19). Conclusions: Our study represents the first gene profiling analysis of LBH transcriptomes in human breast cancer cell lines, with biologic replicates, generated by RNA-seq technology.
2024-05-31 | GSE151206 | GEO
Project description:Background: Higher-order chromatin structure is often perturbed in cancer and other pathological states. Although several genetic and epigenetic differences have been charted between normal and breast cancer tissues, changes in higher-order chromatin organization during tumorigenesis have not been fully explored. To probe the differences in higher-order chromatin structure between mammary epithelial and breast cancer cells, we performed Hi-C analysis on MCF-10A mammary epithelial and MCF-7 breast cancer cell lines. Results: Our studies reveal that the small, gene-rich chromosomes chr16 through chr22 in the MCF-7 breast cancer genome display decreased interaction frequency with each other compared to the inter-chromosomal interaction frequency in the MCF-10A epithelial cells. Interestingly, this finding is associated with a higher occurrence of open compartments on chr16-22 in MCF-7 cells. Pathway analysis of the MCF-7 up-regulated genes located in altered compartment regions on chr16-22 reveals pathways related to repression of WNT signalling. There are also differences in intra-chromosomal interactions between the cell lines; telomeric and sub-telomeric regions in the MCF-10A cells display more frequent interactions than are observed in the MCF-7 cells. Conclusions: We show evidence of an intricate relationship between chromosomal organization and gene expression between epithelial and breast cancer cells. Importantly, this work provides a genome-wide view of higher-order chromatin dynamics and a resource for studying higher-order chromatin interactions in two cell lines commonly used to study the progression of breast cancer.
2015-09-02 | GSE66733 | GEO
Project description:We performed small RNA sequencing in breast cancer cells treated with siRNA for Control, DCGR8, DROSHA, TARBP2, DICER
2018-11-07 | GSE114773 | GEO
Project description:The crosstalk between tumor cells and the adjacent normal epithelium contributes to cancer progression, but its regulators have remained elusive. Here, we show that breast cancer cells maintained in hypoxia release small extracellular vesicles (sEV) that activate mitochondrial dynamics, stimulate mitochondrial movements and promote organelle accumulation at the cortical cytoskeleton in normal mammary epithelial cells. This results in Akt activation, membrane focal adhesion turnover and increased epithelial cell migration. RNA-Seq profiling identified Integrin-Linked Kinase (ILK) as the most upregulated pathway in sEV-treated epithelial cells and genetic or pharmacologic targeting of ILK reversed mitochondrial reprogramming and suppressed sEV-induced cell movements. In a three-dimensional model of mammary gland morphogenesis, sEV treatment induced hallmarks of malignant transformation, with deregulated cell death/cell proliferation, loss of apical-basal polarity and appearance of epithelial-to-mesenchymal transition (EMT) markers. Therefore, sEV released by hypoxic breast cancer cells reprogram mitochondrial dynamics and induce oncogenic changes in a normal mammary epithelium
2020-11-12 | GSE154340 | GEO