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Cancer stem cell subpopulations within the CD44high human breast cancer stem cell compartment

ABSTRACT: The CD44hi compartment in human breast cancer is enriched in tumor-initiating cells, however the functional heterogeneity within this subpopulation remains poorly defined. From a human breast cancer cell line with a known bi-lineage phenotype we have isolated and cloned two CD44hi populations that exhibited mesenchymal/Basal B and luminal/Basal A features, respectively. Rather than CD44+/CD24-,Basal B (G4) cells, only CD44hi/CD24lo, epithelioid Basal A (A4) cells retained a tumor-initiating capacity in NOG mice, form mammospheres and exhibit resistance to standard chemotherapy. Microarray data obtained from Affymetrix Human Gene 1.0 ST Array

ORGANISM(S): Homo sapiens

PROVIDER: GSE32455 | GEO | 2012/06/12

SECONDARY ACCESSION(S): PRJNA147739

REPOSITORIES: GEO

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Cancer stem cell subpopulations within the CD44high human breast cancer stem cell compartment

Project description:The CD44hi compartment in human breast cancer is enriched in tumor-initiating cells, however the functional heterogeneity within this subpopulation remains poorly defined. From a human breast cancer cell line with a known bi-lineage phenotype we have isolated and cloned two CD44hi populations that exhibited mesenchymal/Basal B and luminal/Basal A features, respectively. Rather than CD44+/CD24-,Basal B (G4) cells, only CD44hi/CD24lo, epithelioid Basal A (A4) cells retained a tumor-initiating capacity in NOG mice, form mammospheres and exhibit resistance to standard chemotherapy. Microarray data obtained from Affymetrix Human Gene 1.0 ST Array Five replicates of A4 and 5 replicates of G4

2012-06-11 | E-GEOD-32455 | biostudies-arrayexpress

Cancer stem cells subpopulations within the CD44high human breast cancer stem cell compartment [HMT clones]

Project description:The CD44hi compartment in human breast cancer is enriched in tumor-initiating cells, however the functional heterogeneity within this subpopulation remains poorly defined. From a human breast cancer cell line with a known bi-lineage phenotype we have isolated and cloned CD44hi populations that exhibited mesenchymal/Basal B and luminal/Basal A features, respectively:CD44+/CD24-,Basal B (G4, H6) cells and CD44hi/CD24lo epithelioid Basal A (A4, AB) cells. Seven replicates of A4, seven replicates of G4, three replicates of AB, three replicates of H6

2015-04-30 | E-GEOD-59281 | biostudies-arrayexpress

Cancer stem cells subpopulations within the CD44high human breast cancer stem cell compartment [HMT clones]

2015-04-30 | GSE59281 | GEO

Gene expression profiling of mouse mammary tumorspheres, mammospheres, and mammospheres induced to differentiate

2012-01-30 | GSE32463 | GEO

Gene expression profiling of mouse mammary tumorspheres, mammospheres, and mammospheres induced to differentiate

Project description:Tumorpsheres and mammospheres were used to propagate mouse breast tumor-initiating cells and their normal stem/progenitor counterparts, respectively. Mammospheres induced to differentiate were used to model the more differentiated cells of the mouse mammary gland. We used microarrays to find differentrially expressed genes between tumorspheres, mammospheres, and mammospheres induced to differentiate Primary cells were isolate from either mouse mammary glands (FVB/N) or mouse mammary tumors and placed in stem cell media (MMTV-Neu [N2O2]. Spheres were passaged every 7 days for 3-5 passages and harvested for RNA isolation

2012-01-30 | E-GEOD-32463 | biostudies-arrayexpress

TRIM28 interacts with EZH2 and SWI/SNF to activate genes that promote mammosphere formation

Project description:EZH2 is generally associated with H3K27 methylation and gene silencing. Mass spectrometry of the EZH2-interactome in MCF7 cells revealed EZH2-interactions with SWI/SNF subunits and TRIM28, which formed a complex with EZH2 distinct from PRC2. Transcriptome profiling showed that EZH2 primarily activates transcription in MCF7 cells and with TRIM28 co-regulates a set of genes associated with stem cell maintenance and poor survival of breast cancer patients. TRIM28 depletion repressed EZH2 recruitment and expression of this gene set, in parallel with decreased CD44hi/CD24lo mammosphere formation. These results support PRC2-independent functions of EZH2 and TRIM28 in mammary stem cell enrichment and maintenance.

2017-07-18 | GSE76271 | GEO

Transcriptional profiling of MMTV-tTA/TOP-ICN1 tumor derived cell lines comparing untreated (ICN1-On) cells to 24-hour doxcycline treated (ICN1-Off) samples

2011-12-05 | GSE34146 | GEO

Obesity Promotes Epithelial-To-Mesenchymal Transition and Tumor Progression in a Mouse Model of Claudin-Low Breast Cancer.

Project description:ABSTRACT: Obesity is responsible for decreased overall survival for breast cancer patients. Here, we describe the generation, characterization and application of a novel murine mammary tumor initiating cell model (M-Wnt) that recapitulates the claudin-low subtype of human breast cancer and permits the study of TIC’s in wild-type, immunocompetent mice. M-Wnt cells readily form mammospheres in suspension culture, express markers consistent with epithelial-to-mesenchymal transition (EMT), and generate claudin-low mammary tumors when as few as 50 cells are orthotopically injected. Using the M-Wnt cell lines in tandem with a more basal-like epithelial breast cancer cell line, E-Wnt, we found that diet induced obesity significantly downregulates epithelial markers, such as E-cadherin, and upregulates mesenchymal markers including fibronectin, N-cadherin, SNAIL, Oct-4, and TGF-b. This reveals a previously unidentified link between energy balance and EMT. The ability of calorie restriction (CR) to reverse EMT, upregulate epithelial markers and downregulate mesenchymal markers indicates the plasticity of the TICs, as well as the potential importance of lifestyle modifications as cancer prevention strategies. 28 array samples

2012-06-29 | E-GEOD-28713 | biostudies-arrayexpress

Transcriptional profiling of MMTV-tTA/TOP-ICN1 tumor derived cell lines comparing untreated (ICN1-On) cells to 24-hour doxcycline treated (ICN1-Off) samples

Project description:NOTCH activation has been recently implicated in human basal-like breast cancers associated with a poor prognosis. To address the role of Notch1 in mammary transformation and mammary tumor initiating cell activity, we developed a doxycycline-regulated model of Notch1-mediated mammary transformation. These mice develop mammary adenocarcinomas that express cytokeratin (CK) 8/18 and contain rare cells that also express keratin 14. In vivo limiting dilution analyses reveal that these mammary tumors exhibit functional heterogeneity and harbor a rare (1/2978) mammary tumor initiating cell population. Using this dox-regulated Notch1 mammary tumor model, we demonstrate that Notch1 inhibition results in mammary tumor regression in vivo and prevents disease recurrence in 4 of 6 tumors tested. Consistent with the in vivo data, Notch1 inhibition reduces mammary tumorsphere forming activity in vitro. Using doxycycline-responsive tumor derived cell lines, we also identify the embryonic stem cell transcription factor Nanog as a novel Notch1-regulated gene in mammospheres. These data indicate that Notch1 contributes to mammary tumor initiating activity and raises the possibility that NOTCH therapeutics may have efficacy in human basal-like breast cancers associated with NOTCH activation. Primary mammary tumors were isolated from two different MMTV-tTA/TOP-ICN1 transgenic mice, minced, enzymatically digested and converted to culture. To identify changes in gene expression in response to ICN1 suppression, tumor-derived cell lines 8534 and 8542 were left untreated (8534-Untreated; 8542-Untreated) or treated with 2ug/ml doxycycline for 24 hours (8534-Dox; 8542-Dox). Cells were collected by scraping and total RNA was isolated, followed by real-time PCR validation of NOTCH1 target gene modulation. RNA samples were further hybridized to Affymetrix mouse genome 430A2.0 arrays.

2011-12-05 | E-GEOD-34146 | biostudies-arrayexpress

Obesity Promotes Epithelial-To-Mesenchymal Transition and Tumor Progression in a Mouse Model of Claudin-Low Breast Cancer.

2012-06-30 | GSE28713 | GEO

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