Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA177955 | ENA |
REPOSITORIES: ENA
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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 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:Global proteomic profiling of three mammary epithelial cell types in normal human breast tissue. Primary breast specimens were obtained from 10 women undergoing reduction mammoplasties. Clinical co-variates include age (28-67), hormone status (follicular, luteal, post-menopausal) and mammary epithelial cell type (basal, luminal progenitor, mature luminal).
2021-03-12 | MSV000087042 | MassIVE
Project description:Basal breast cancers, an aggressive breast cancer subtype that has poor treatment options, are thought to arise from luminal mammary epithelial cells that undergo basal-like plasticity through poorly understood mechanisms. Using genetic mouse models and ex vivo primary organoid cultures, we show that conditional co-deletion of the LATS1 and LATS2 kinases, key effectors of Hippo pathway signaling, in mature mammary luminal epithelial cells promotes the development of basal-like carcinomas that metastasize over time. Genetic co-deletion experiments revealed that phenotypes resulting from the loss of LATS1/2 activity are dependent on the transcriptional regulators YAP/TAZ. Notably, transcriptional analyses of LATS1/2-deleted mammary epithelial cells revealed a gene expression program that associates with human basal breast cancers. Our study demonstrates in vivo roles for the LATS1/2 kinases in mammary epithelial homeostasis and luminal-basal fate control and implicates signaling networks induced upon the loss of LATS1/2 activity in the development of basal breast cancers.
2022-09-26 | GSE196555 | GEO
Project description:Porcine mammary fatty tissues represent an abundant source of biomaterial for generation of breast-specific extracellular matrix (ECM). Here we report the extraction of total ECM proteins from pig breast fatty tissues, the fabrication of hydrogel scaffolds from the extracted ECM proteins, the structural properties of the scaffolds, and the applications of the hydrogel in human mammary epithelial cell spatial cultures for cell surface receptor expression, metabolomics characterization, acini formation, proliferation, migration between different scaffolding compartments, and in vivo tumor formation. This model system provides an additional option for studying human breast diseases such as breast cancer.
2019-11-12 | PXD010960 | Pride
Project description:The goal of this study is to identify the DNA methylation changes caused by exposure of to the DNMT inhibitor 5-aza-2â-deoxycytidine (5Aza) and HDAC inhibitor Trichostatin A (TSA). We performed whole-genome bisulfite sequencing of the drug-treated MCF7 breast cancer cell lines and compare their DNA methylation profile with the untreated MCF7 (see E-MTAB-2014). While MCF7 treated with both drugs experienced global loss of DNA methylation, the 5Aza induced stronger demethylation than TSA.
2016-06-30 | E-MTAB-3785 | biostudies-arrayexpress
Project description:Growing interest in the cellular origins of different breast cancer subtypes has prompted investigations into the subpopulations of the normal breast epithelia and their differentiation hierarchy. Several groups have demonstrated a likely luminal-progenitor cell origin for basal-like breast cancer. However, the molecular and cellular mechanisms underlying why one breast cell type might be more susceptible to transformation are yet to be elucidated. To observe the molecular differences in the different cell subpopulation response to ionizing radiation (IR), we performed gene expression profiling of MUC1+-sorted and CD10+-sorted primary human mammary epithelial cell cultures. Transcriptional response was measured at 2 and 24 hr after treatment with 2 and 5 Gy IR using Illumina HumanHT-12 v4 Expression Beadchips. The complete sample cohort included time-point matched untreated (0 Gy) controls in a total of 5 individual patients. Our analyses indicated several cell-type specific differences in response to IR. RNA was extracted from MUC1+-sorted and CD10+-sorted primary human mammary epithelial cell cultures at 2 and 24 hr after treatment with 0, 2, and 5 Gy ionizing radiation (12 samples per patient), in a total of 5 individual patients.
2016-02-07 | E-GEOD-67595 | biostudies-arrayexpress
Project description:Cancer prevention has a profound impact on cancer-associated mortality and morbidity. We previously identified TGFβ signaling as a candidate regulator of mammary epithelial cells associated with breast cancer risk. Here, we show that short-term TGFBR inhibitor (TGFBRi) treatment of peripubertal ACI inbred and Sprague Dawley outbred rats induces lasting changes and prevents estrogen- and carcinogen-induced mammary tumors, respectively. We identify TGFBRi-responsive cell populations by single cell RNA-sequencing, including a unique epithelial subpopulation designated secretory basal cells (SBCs) with progenitor features. We detect SBCs in normal human breast tissues and find them to be associated with breast cancer risk. Interactome analysis identifies SBCs as the most interactive cell population and the main source of insulin-IGF signaling. Accordingly, inhibition of TGFBR and IGF1R decrease proliferation of organoid cultures. Our results reveal a critical role for TGFβ in regulating mammary epithelial cells relevant to breast cancer and serve as a proof-of-principle cancer prevention strategy.
2022-11-02 | GSE184095 | GEO
Project description:Tumor cells interact with the microenvironment that specifically supports and promotes tumor development. Key components in the tumor environment have been linked to various aggressive cancer features and can further influence the presence of subpopulations of cancer cells with specific functions, including cancer stem cells and migratory cells. To model and further understand the influence of specific microenvironments we have developed an experimental platform using cell-free patient-derived scaffolds (PDSs) from primary breast cancers infiltrated with standardized breast cancer cell lines. This PDS culture system induced a series of orchestrated changes in differentiation, epithelial-mesenchymal transition, stemness and proliferation of the cancer cell population, where an increased cancer stem cell pool was confirmed using functional assays. Furthermore, global gene expression profiling showed that PDS cultures were similar to xenograft cultures. Mass spectrometry analyses of cell-free PDSs identified subgroups based on their protein composition that were linked to clinical properties, including tumor grade. Finally, we observed that an induction of epithelial-mesenchymal transition-related genes in cancer cells growing on the PDSs were significantly associated with clinical disease recurrences in breast cancer patients. Patient-derived scaffolds thus mimics in vivo-like growth conditions and uncovers unique information about the malignancy-inducing properties of tumor microenvironment.
2020-06-25 | PXD018367 | Pride
Project description:The goal of this study is to identify the gene expression changes caused by exposure of to the DNMT inhibitor 5-aza-2'-deoxycytidine (5Aza) and HDAC inhibitor Trichostatin A (TSA). We performed rRNA-depleted RNA sequencing of the untreated and drug-treated MCF7 breast cancer cell lines and carried out differential gene expression analysis. Although 5Aza caused a stranger demethylation effect than TSA, there were fewer differentially expressed gene in the 5Aza-treated MCF7 than the TSA-treated cells.
2016-06-30 | E-MTAB-3794 | biostudies-arrayexpress