Hormonal and nutritive control of HCC1937 basal cell line plasticity
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE85469 | GEO | 2016/08/12
SECONDARY ACCESSION(S): PRJNA338598
REPOSITORIES: GEO
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Project description:Purpose: To compare the transcriptomes of HCC1937 vector and wtBRCA1 cells which were treated with OTX-015. Methods: HCC1937 vector and wtBRCA1 cells were treated with 5 micromolar OTX-015 for 24 hours. Total RNA was extracted and processed with NEBNext Ultra Directional RNA Library Prep Kit for cDNA library preparation. The data are in duplicate and raw data were generated by Illumina 2500 sequencer. The Fastq format data were then processed with Tophat for genome mapping. After getting the bam files, they were further analyzed with cuffdiff for gene expression of different groups. Results: From the transcriotome profiling and analysis, we got gene expression data of DMSO control group and OTX-015 treatment group for the HCC1937 BRCA1 isogenic cell lines. Conclusion: The gene expression data revealed the transcriptome variation by OTX-015 treatment.
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Project description:Airway hillocks are stratified epithelial structures of unknown function. We show that the luminal cells of hillocks are squamous barrier cells that shield a unique population of underlying hillock basal stem cells. Hillocks occur in characteristic locations and persist for months in uninjured mice. Following injury, hillock basal stem cells undergo massive clonal expansion, resurface denuded airway, and demonstrate extreme plasticity, generating classic airway epithelium with its six component cell types. Remarkably, hillocks resist a very broad spectrum of injuries, including toxins, infection, acid, and physical injury. Furthermore, hillock basal stem cells are characterized by enhanced expression associated with barrier function, cell adhesion, and retinoic acid catabolism. Indeed, hillock basal cells preferentially expand, stratify, and keratinize in the setting of retinoic acid signaling inhibition, a known clinical cause of squamous metaplasia. Finally, we identify human hillocks whose basal cells demonstrate preferential sensitivity to retinoic acid inhibition and conserved barrier properties. Given their capacity for clonal expansion, their plasticity, and their retinoic acid sensitivity, the existence of hillocks and hillock basal stem cells have broad implications for injury repair and for defining the origin of squamous metaplasia, long thought to be a precursor of lung cancer.
2024-03-05 | GSE253020 | GEO
Project description:Airway hillocks are stratified epithelial structures of unknown function. We show that the luminal cells of hillocks are squamous barrier cells that shield a unique population of underlying hillock basal stem cells. Hillocks occur in characteristic locations and persist for months in uninjured mice. Following injury, hillock basal stem cells undergo massive clonal expansion, resurface denuded airway, and demonstrate extreme plasticity, generating classic airway epithelium with its six component cell types. Remarkably, hillocks resist a very broad spectrum of injuries, including toxins, infection, acid, and physical injury. Furthermore, hillock basal stem cells are characterized by enhanced expression associated with barrier function, cell adhesion, and retinoic acid catabolism. Indeed, hillock basal cells preferentially expand, stratify, and keratinize in the setting of retinoic acid signaling inhibition, a known clinical cause of squamous metaplasia. Finally, we identify human hillocks whose basal cells demonstrate preferential sensitivity to retinoic acid inhibition and conserved barrier properties. Given their capacity for clonal expansion, their plasticity, and their retinoic acid sensitivity, the existence of hillocks and hillock basal stem cells have broad implications for injury repair and for defining the origin of squamous metaplasia, long thought to be a precursor of lung cancer.
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Project description:In order to identify new targets for basal-like breast cancers, we performed Methyl-Seq of 10 breast cancer cell lines. Basal-like cell lines (MDAMB231, MDAMB436, HCC1937, SUM149, SUM1315 and MCF10A) were compared to luminal cell lines (MCF7 and T47D). Moreover we could also study BRCA1 influence on methylome of basal-like breast cancer. 4 of our cell lines are indeed BRCA1 mutated (MDAMB436, HCC1937, SUM149 and SUM1315) and we also developed 2 cell lines that come from the BRCA1 mutated SUM1315 cell line stably transfected with empty LXSN plasmid (SUM1315-LXSN) or with a BRCA1 coding plasmid (SUM1315-BRCA1).
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Project description:Stem cell-based models of human heart tissue and cardiac differentiation employ monolayer and 3D organoid cultures with different properties, cell type composition, and maturity. Here we show how cardiac monolayer, embryoid body, and engineered heart tissue trajectories compare in a single-cell roadmap of atrial and ventricular differentiation conditions. Using a multiomic approach and gene-regulatory network inference, we identified regulators of the epicardial, atrial and ventricular cardiomyocyte lineages. We identified ZNF711 as a regulatory switch and safeguard for cardiomyocyte commitment. We show that ZNF711 ablation prevents cardiomyocyte differentiation in the absence of retinoic acid, causing progenitors to be diverted more prominently to epicardial and other lineages. Retinoic acid rescues this shift in lineage commitment and promotes atrial cardiomyocyte differentiation by regulation of shared and complementary target genes, showing an interplay between ZNF711 and retinoic acid in cardiac lineage commitment.
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Project description:Stem cell-based models of human heart tissue and cardiac differentiation employ monolayer and 3D organoid cultures with different properties, cell type composition, and maturity. Here we show how cardiac monolayer, embryoid body, and engineered heart tissue trajectories compare in a single-cell roadmap of atrial and ventricular differentiation conditions. Using a multiomic approach and gene-regulatory network inference, we identified regulators of the epicardial, atrial and ventricular cardiomyocyte lineages. We identified ZNF711 as a regulatory switch and safeguard for cardiomyocyte commitment. We show that ZNF711 ablation prevents cardiomyocyte differentiation in the absence of retinoic acid, causing progenitors to be diverted more prominently to epicardial and other lineages. Retinoic acid rescues this shift in lineage commitment and promotes atrial cardiomyocyte differentiation by regulation of shared and complementary target genes, showing an interplay between ZNF711 and retinoic acid in cardiac lineage commitment.
2025-01-27 | GSE263193 | GEO
Project description:Stem cell-based models of human heart tissue and cardiac differentiation employ monolayer and 3D organoid cultures with different properties, cell type composition, and maturity. Here we show how cardiac monolayer, embryoid body, and engineered heart tissue trajectories compare in a single-cell roadmap of atrial and ventricular differentiation conditions. Using a multiomic approach and gene-regulatory network inference, we identified regulators of the epicardial, atrial and ventricular cardiomyocyte lineages. We identified ZNF711 as a regulatory switch and safeguard for cardiomyocyte commitment. We show that ZNF711 ablation prevents cardiomyocyte differentiation in the absence of retinoic acid, causing progenitors to be diverted more prominently to epicardial and other lineages. Retinoic acid rescues this shift in lineage commitment and promotes atrial cardiomyocyte differentiation by regulation of shared and complementary target genes, showing an interplay between ZNF711 and retinoic acid in cardiac lineage commitment.
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2014-01-12 | E-MEXP-3833 | biostudies-arrayexpress
Project description:Publication includes a mathematical model for how retinoic acid affects thrombomodulin gene and mRNA expression as well as a two-compartment pharmacokinetic model for retinoic acid.
2020-03-16 | MODEL1907140001 | BioModels