Effect of laminin adhesion on basal human mammary epithelial cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA812925 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18230384.fastq.gz | Fastqsanger.gz | |||
| SRR18230385.fastq.gz | Fastqsanger.gz | |||
| SRR18230386.fastq.gz | Fastqsanger.gz | |||
| SRR18230387.fastq.gz | Fastqsanger.gz | |||
| SRR18230388.fastq.gz | Fastqsanger.gz |
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Project description:Mammary epithelium is composed by luminal and basal epithelial cells, which are adhere to the basement membrane (BM). To dissect how basal cell functions are regulated by BM laminin adhesion, we performed RNA sequencing of basal human mammary epithelial cells adhered on laminin-111, -421 or -521 coated cell culture plates for 48 hours.
2022-11-07 | GSE197950 | GEO
Project description:Integrin dimers a3/b1, a6/b1 and a6/b4 are the receptors of mammary epithelial cells for Laminin, major component of the mammary basement membrane. Antibodies against a6 and a3 integrin chains serve to isolate stem cell enriched populations from mammary epithelium, however, role of integrin dimers comprising these chains in the control of mammary stem cell activity are not known. To investigate the role of Laminin-binding integrins in the control of mammary stem cell function, a3 and a6 chains were deleted from mammary basal cells in vitro using Cre-recombinase carrying adenovirus. We found that deletion of single integrin chain (either a3, or a6) did not significantly affect stem cell potential as evaluated by transplantation and mammosphere assays, whereas basal cells depleted of both a3 and a6 integrin chains (a3a6KO) presented severely diminished stem cell activity. In this study the transcriptional profiles of a3a6KO were analysed and compared to those of control cells.
2019-04-23 | GSE117120 | 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:Background Annexin-1 (ANXA1) plays pivotal roles in regulating various physiological processes including inflammation, proliferation and apoptosis, and deregulations of ANXA1 functions have been associated with tumorigenesis and metastasis events in several cancers. Though ANXA1 levels correlate with breast cancer disease status and outcome, its distinct functional involvement in breast cancer initiation and progression remains unclear. We hypothesized ANXA1-responsive kinase signaling alteration and associated phosphorylation signaling underlie early events in breast cancer initiation events and hence profiled ANXA1-dependent phosphorylation changes in mammary gland epithelial cells. Methods Quantitative phosphoproteomics analysis of mammary gland epithelial cells derived from ANXA1-heterozygous and ANXA1-deficient mice was carried out using SILAC-based mass spectrometry. Kinase and signaling changes underlying ANXA1 perturbations were derived by upstream kinase prediction and integrated network analysis of altered proteins and phosphoproteins. Results We identified a total of 8,110 unique phosphorylation sites, of which 582 phosphorylation sites on 372 proteins showed ANXA1-responsive changes. A majority of these phosphorylation changes occurred on proteins associated with cytoskeletal reorganization spanning the focal adhesion, stress fibers, and also the microtubule network pressing on new roles for ANXA1 in regulating microtubule dynamics. Comparative analysis of regulated global proteome and phosphoproteome highlighted key differences in translational and post-translational effects of ANXA1, and stressed on a close-coordinated rewiring of the cell adhesion network. Kinase prediction analysis suggested activity modulation of CAMK2, PAK, ERK, and IKK kinases upon loss of ANXA1. Integrative analysis revealed regulation of WNT and also Hippo signaling pathways in ANXA1-deficient mammary epithelial cells, wherein there is a downregulation of transcriptional effects of TEAD suggestive of ANXA1-responsive transcriptional rewiring. Conclusions The phosphoproteome landscape uncovered several novel perspectives for ANXA1 in mammary gland biology and stressed on its involvement in key signaling pathways modulating cell adhesion and migration that could contribute to breast cancer initiation.
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Project description:We report the application of Single-Cell RNA-Sequencing technology for high-throughput profiling in mammary basal epithelial cells of WT and Fgd5-depeleted mice. By obtaining basal epithelial cells isolated from mammary gland of WT and Fgd5-depeleted mice, we performed Single-Cell RNA-Sequencing of basal epithelial cells. The scRNA-Seq libraries were prepared with Single Cell 3′ Reagent Kit v2 (10×Genomics) following the user guide provided. We found that FGD5 promotes mammary development by maintaining LGR5/SLPI/ID3 positive basal cell subsets.. We conclude that Single-Cell RNA-Sequencing would expedite genetic network analyses and permit the dissection of complex biologic functions.
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Project description:Bovine mammary epithelial cells in response to artemisinin treatment
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Project description:The following data comes from two separate experiments. In the initial experiment, luminal and basal murine mammary epithelial cells were analyzed by reduced representation bisulfite sequencing (RRBS) to generate methylome profiles. In the second experiment, luminal and basal murine mammary epithelial cells were analyzed by ATAC-seq.
2018-06-10 | GSE80181 | GEO
Project description:Three well-known tumor suppressors, TRP53, p16INK4a, and p19ARF (p16INK4a and p19ARF are both coded by the gene Cdkn2a) have been connected to the limiting of stem cell self-renewal and proliferation in some tissues. Here we deposit RNA microarray expression data of sorted mouse Krt14-cre mT/mG Trp53f/f Cdkn2a-/- mammary epithelial basal cells and their wild type control cells (Krt14-cre mT/mG).
2021-01-02 | GSE137573 | GEO
Project description:Molecular/cellular events that associate with epithelial-to-mesenchymal transition (EMT) are linked to acquisition of cancer stem cell traits, but whether EMT mechanisms regulate tissue epithelial cell fate and stem cell activity in vivo remains ambiguous. Using single-cell RNA sequencing, we detect heterogeneous EMT gene expression in stem cell-containing mammary basal/myoepithelial cells that normally possess both epithelial and smooth muscle characteristics. We show that EMT-inducing transcription factor Zeb1 is required within the mammary epithelium for ductal branching morphogenesis and regeneration, and that it promotes basal cell fate and regulates stem cell proliferation dynamics. We provide genetic and molecular evidence for EMT-dependent and -independent mechanisms of Zeb1 function, and show that Zeb1 cooperates with YAP to directly activate targets that inhibit Wnt signaling or control cell cycle. Together, our findings underscore Zeb1-mediated EMT control in governing mammary basal cell fate and proliferative activity, but with an interesting turn that involves mechanisms beyond EMT.
2022-03-08 | GSE188781 | GEO