Single Cell Analysis of Mouse Lung Epcam+CD31/34/45- Epithelial Cells
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ABSTRACT:
PROVIDER: PRJNA476235 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7346121.fastq.gz | Fastqsanger.gz |
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Project description:Epithelial cell homeostasis and renewal in the lung requires the supportive signals from surrounding mesenchymal cells. Single cell RNA-seq analysis was used to examine the gene expression levels of several receptors on the Sftpc+ alveolar type II stem cells. Single cell RNA-seq revealed Ghr, Cxcr2, Cxcr4, and Igf1r expressing cells were all Sftpc+ cells in the normal mouse lung.
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Project description:We analysed the signature of sorted CD45-CD31-Ter119-EpCAM+ lung epithelial cells and CD45-CD31-Ter119-EpCAM- lung mesenchymal cells from the control vs. irradiated lungs of BALB/c mice.
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Project description:Human mucosa was collected from two different individuals undergoing colectomy. After treatment with EDTA, colonic crypts were isolated and further dis-aggregated using Dispase. Next, cells were stained using antibodies directed against the extracellular domain of EpCAM, PTK7, CD11, CD31, and CD45. Cells were analyzed and sorted via flow cytometry (BD Aria). After excluding non-epithelial cells (Epcam. CD11, CD31, and CD45 negative), the EpCAM positive fraction was divided into fractions expressing either high, medium, low, or negative levels of PTK7. Sorted cells were transferred to Trizol for RNA extraction and RNA was purified using the Qiagen RNA Mini Kit.
2016-01-12 | GSE68340 | GEO
Project description:Introduction: The Epithelial Cell Adhesion Molecule (EpCAM) has been shown to be strongly expressed in human breast cancer and cancer stem cells and its overexpression has been supposed to support tumor progression and metastasis. However, effects of EpCAM overexpression on normal breast epithelial cells have never been studied before. Therefore, we analyzed effects of transient adenoviral overexpression of EpCAM on proliferation, migration and differentiation of primary human mammary epithelial cells (HMECs). METHODS: HMECs were transfected by an adenoviral system for transient overexpression of EpCAM. Thereafter, changes in cell proliferation and migration were studied using a real time measurement system. Target gene expression was evaluated by transcriptome analysis in proliferating and polarized HMEC cultures. A Chicken Chorioallantoic Membrane (CAM) xenograft model was used to study effects on in vivo growth of HMECs. RESULTS: EpCAM overexpression in HMECs did not significantly alter gene expression profile of proliferating or growth arrested cells. Proliferating HMECs displayed predominantly glycosylated EpCAM isoforms and were inhibited in cell proliferation and migration by upregulation of p27KIP1 and p53. HMECs with overexpression of EpCAM showed a down regulation of E-cadherin. Moreover, cells were more resistant to TGF-beta1 induced growth arrest and maintained longer capacities to proliferate in vitro. EpCAM overexpressing HMECs xenografts in chicken embryos showed hyperplastic growth, lack of lumen formation and increased infiltrates of the chicken leukocytes. CONCLUSIONS: EpCAM revealed oncogenic features in normal human breast cells by, inducing resistance to TGF-beta1-mediated growth arrest and supporting a cell phenotype with longer proliferative capacities in vitro. EpCAM overexpression resulted in hyperplastic growth in vivo. Thus, we suggest that EpCAM acts as a prosurvival factor counteracting terminal differentiation processes in normal mammary glands. Differential expression was assessed with the moderated t-test (Bioconductor's limma package) with pairing of the samples by the donor. Raw p-values were adjusted for multiple hypothesis testing using the method from Benjamini and Hochberg for a strong control of the false discovery rate. EPCAM and GFP over-expression in proliferating mammary epithelial cells from two donors (6 and 8). Expression levels between EPCAM and control samples were compared to determine whether, and to which extent EPCAM over-expression alters the gene expression profile of the cells.
2013-06-13 | E-GEOD-39071 | biostudies-arrayexpress
Project description:We collected freshly sorted mesenchyme (live CD45-Epcam-CD31-PDGFRa+GFP- or GFP+) from dissociated lung tissue of INKBRITE animals to characterize the transcriptome difference between p16INK4a+ vs p16INK4a- cells at homeostasis and during injury. We used fluorescence activated cell sorting (FACS) to exclude immune (CD45+), epithelial (Epcam+), and endothelial (CD31+) cells and positively select for PDGFRa+ mesenchyme. Cells were sequenced at a depth of average of 45 million reads/sample. The results revealed an increase of senescence associated secretory phenotype (SASP) signature in p16INK4+ cells that becomes refined after injury. We found the expression of an epithelial growth factor epiregulin (ereg) increased in p16INK4a+ cells after injury suggesting a possible role of p16INK4a+ senescence during regeneration of lung epithelium.
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Project description:Background: The Epithelial Cell Adhesion Molecule (EpCAM) has been shown to be strongly expressed in human breast cancer and cancer stem cells and its overexpression has been supposed to support tumor progression and metastasis. However, effects of EpCAM overexpression on normal breast epithelial cells have never been studied before. Therefore, we analyzed effects of transient adenoviral overexpression of EpCAM on proliferation, migration and differentiation of primary human mammary epithelial cells (HMECs). METHODS: HMECs were transfected by an adenoviral system for transient overexpression of EpCAM. Thereafter, changes in cell proliferation and migration were studied using a real time measurement system. Target gene expression was evaluated by transcriptome analysis in proliferating and polarized HMEC cultures. A Chicken Chorioallantoic Membrane (CAM) xenograft model was used to study effects on in vivo growth of HMECs. RESULTS: EpCAM overexpression in HMECs did not significantly alter gene expression profile of proliferating or growth arrested cells. Proliferating HMECs displayed predominantly glycosylated EpCAM isoforms and were inhibited in cell proliferation and migration by upregulation of p27KIP1 and p53. HMECs with overexpression of EpCAM showed a down regulation of E-cadherin. Moreover, cells were more resistant to TGF-beta1 induced growth arrest and maintained longer capacities to proliferate in vitro. EpCAM overexpressing HMECs xenografts in chicken embryos showed hyperplastic growth, lack of lumen formation and increased infiltrates of the chicken leukocytes. CONCLUSIONS: EpCAM revealed oncogenic features in normal human breast cells by, inducing resistance to TGF-beta1-mediated growth arrest and supporting a cell phenotype with longer proliferative capacities in vitro. EpCAM overexpression resulted in hyperplastic growth in vivo. Thus, we suggest that EpCAM acts as a prosurvival factor counteracting terminal differentiation processes in normal mammary glands.
2013-06-20 | GSE37172 | GEO
Project description:Background: The Epithelial Cell Adhesion Molecule (EpCAM) has been shown to be strongly expressed in human breast cancer and cancer stem cells and its overexpression has been supposed to support tumor progression and metastasis. However, effects of EpCAM overexpression on normal breast epithelial cells have never been studied before. Therefore, we analyzed effects of transient adenoviral overexpression of EpCAM on proliferation, migration and differentiation of primary human mammary epithelial cells (HMECs). METHODS: HMECs were transfected by an adenoviral system for transient overexpression of EpCAM. Thereafter, changes in cell proliferation and migration were studied using a real time measurement system. Target gene expression was evaluated by transcriptome analysis in proliferating and polarized HMEC cultures. A Chicken Chorioallantoic Membrane (CAM) xenograft model was used to study effects on in vivo growth of HMECs. RESULTS: EpCAM overexpression in HMECs did not significantly alter gene expression profile of proliferating or growth arrested cells. Proliferating HMECs displayed predominantly glycosylated EpCAM isoforms and were inhibited in cell proliferation and migration by upregulation of p27KIP1 and p53. HMECs with overexpression of EpCAM showed a down regulation of E-cadherin. Moreover, cells were more resistant to TGF-beta1 induced growth arrest and maintained longer capacities to proliferate in vitro. EpCAM overexpressing HMECs xenografts in chicken embryos showed hyperplastic growth, lack of lumen formation and increased infiltrates of the chicken leukocytes. CONCLUSIONS: EpCAM revealed oncogenic features in normal human breast cells by, inducing resistance to TGF-beta1-mediated growth arrest and supporting a cell phenotype with longer proliferative capacities in vitro. EpCAM overexpression resulted in hyperplastic growth in vivo. Thus, we suggest that EpCAM acts as a prosurvival factor counteracting terminal differentiation processes in normal mammary glands. For each gene a representative transcript probe set was selected based on a score that combines average expression and variation of expression across all samples. Transcript probe sets with more than 4 probes were preferred. Differential expression analysis between EPCAM over-expressing and control cells (expressing GFP) was performed using a paired moderated t-test employing functions provided by Bioconductor's limma package. p-values were subsequently adjusted for multiple hypothesis testing using the method from Benjamini and Hochberg for a strong control of the false discovery rate.
2013-06-20 | E-GEOD-37172 | biostudies-arrayexpress
Project description:Introduction: The Epithelial Cell Adhesion Molecule (EpCAM) has been shown to be strongly expressed in human breast cancer and cancer stem cells and its overexpression has been supposed to support tumor progression and metastasis. However, effects of EpCAM overexpression on normal breast epithelial cells have never been studied before. Therefore, we analyzed effects of transient adenoviral overexpression of EpCAM on proliferation, migration and differentiation of primary human mammary epithelial cells (HMECs). METHODS: HMECs were transfected by an adenoviral system for transient overexpression of EpCAM. Thereafter, changes in cell proliferation and migration were studied using a real time measurement system. Target gene expression was evaluated by transcriptome analysis in proliferating and polarized HMEC cultures. A Chicken Chorioallantoic Membrane (CAM) xenograft model was used to study effects on in vivo growth of HMECs. RESULTS: EpCAM overexpression in HMECs did not significantly alter gene expression profile of proliferating or growth arrested cells. Proliferating HMECs displayed predominantly glycosylated EpCAM isoforms and were inhibited in cell proliferation and migration by upregulation of p27KIP1 and p53. HMECs with overexpression of EpCAM showed a down regulation of E-cadherin. Moreover, cells were more resistant to TGF-beta1 induced growth arrest and maintained longer capacities to proliferate in vitro. EpCAM overexpressing HMECs xenografts in chicken embryos showed hyperplastic growth, lack of lumen formation and increased infiltrates of the chicken leukocytes. CONCLUSIONS: EpCAM revealed oncogenic features in normal human breast cells by, inducing resistance to TGF-beta1-mediated growth arrest and supporting a cell phenotype with longer proliferative capacities in vitro. EpCAM overexpression resulted in hyperplastic growth in vivo. Thus, we suggest that EpCAM acts as a prosurvival factor counteracting terminal differentiation processes in normal mammary glands. Differential expression was assessed with the moderated t-test (Bioconductor's limma package) with pairing of the samples by the donor. Raw p-values were adjusted for multiple hypothesis testing using the method from Benjamini and Hochberg for a strong control of the false discovery rate.
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Project description:Epithelial (CD31-CD45-EpCAM+) and stromal (CD31-CD45-EpCAM-) lung cells were derived by FACS from ShhCre;Ezh2fl/fl and control ShhCre;Ezh2fl/+ mouse embryos at day E16.5 (3 biological replicates per genotype-tissue combination). Total RNA extracted from the samples was subjected to NGS library preparation using TruSeq Stranded Total RNA with Ribo-Zero (Illumina). Completed libraries from different samples were sequenced on HiSeq 2000 TruSeq with SBS Kit v3 - HS reagents (Illumina) as 100 bp single end reads at the Australian Genome Research Facility. RNA-seq gene expression profiles from Ezh2 deficient and control lung epithelial and stromal cell populations at day E16.5 (3 replicates per genotype-tissue combination).
2015-05-11 | E-GEOD-57391 | biostudies-arrayexpress