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The role of p53 in the regulation of miRNA expression profiling

ABSTRACT: To understand the role of p53 in regulating stem cell population (CD24-CD44+) and stemness-associated miRNAs, we first compared miRNA expression profiles between human mammary epithelial cells knocked-down p53 and control cells. We then cross-referenced p53-regulated miRNAs with stemness-associated miRNAs analyzed from expression profiling of sorted CD24-CD44+ and non-CD24-CD44+ cell populations. Further biological experiments were performed with the miRNAs that are altered in CD24-CD44+ stem cell populations and also regulated by p53.

ORGANISM(S): Merkel cell polyomavirus Rattus norvegicus Mus musculus Human gammaherpesvirus 8 Human alphaherpesvirus 1 JC polyomavirus Betapolyomavirus macacae Murid gammaherpesvirus 4 Homo sapiens Human immunodeficiency virus 1 Human betaherpesvirus 5 Human alphaherpesvirus 2 Betapolyomavirus hominis human gammaherpesvirus 4 Murid betaherpesvirus 1

PROVIDER: GSE25035 | GEO | 2011/02/01

SECONDARY ACCESSION(S): PRJNA142751

REPOSITORIES: GEO

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miRNA expression profiling in human mammary epithelial cell (HMEC) CD24-CD44+ and non-CD24-CD44+ cell populations

2011-02-01 | GSE25036 | GEO

miRNA expression profiling in human mammary epithelial cell (HMEC) CD24-CD44+ and non-CD24-CD44+ cell populations

Project description:To understand the role of p53 in regulating stem cell population (CD24-CD44+) and stemness-associated miRNAs, we first compared miRNA expression profiles between human mammary epithelical cells knocked-down p53 and control cells. We then cross-referenced p53-regulated miRNAs with stemness-associated miRNAs analyzed from expression profiling of sorted CD24-CD44+ and non-CD24-CD44+ cell populations. Further biological experiments were performed with the miRNAs that are altered in CD24-CD44+ stem cell populations and also regulated by p53. Total RNAs, including miRNAs, extracted from CD24-CD44+ cells (labeled in Hy3) and non-CD24-CD44+ cells (labeled in Hy5) were hybridized on Exiqon miRCURY LNA arrays according to the manufacturer's protocol.

2011-02-01 | E-GEOD-25036 | biostudies-arrayexpress

The role of p53 in the regulation of miRNA expression profiling

Project description:To understand the role of p53 in regulating stem cell population (CD24-CD44+) and stemness-associated miRNAs, we first compared miRNA expression profiles between human mammary epithelial cells knocked-down p53 and control cells. We then cross-referenced p53-regulated miRNAs with stemness-associated miRNAs analyzed from expression profiling of sorted CD24-CD44+ and non-CD24-CD44+ cell populations. Further biological experiments were performed with the miRNAs that are altered in CD24-CD44+ stem cell populations and also regulated by p53. Total RNAs, including miRNAs, were extracted from cells infected with retrovirus expressing shp53 (labeled in Hy3) and vector control (labeled in Hy5). miRNAs were hybridized on Exiqon miRCURY LNA arrays according to the manufacturer's protocol.

2011-02-01 | E-GEOD-25035 | biostudies-arrayexpress

p53 regulates epithelial-mesenchymal transition (EMT) and stem cell properties through modulation of miRNAs.

Project description:This SuperSeries is composed of the following subset Series: GSE25035: The role of p53 in the regulation of miRNA expression profiling GSE25036: miRNA expression profiling in human mammary epithelial cell (HMEC) CD24-CD44+ and non-CD24-CD44+ cell populations Refer to individual Series

2011-02-01 | E-GEOD-25037 | biostudies-arrayexpress

c-Src functionality controls self-renewal, tumorigenicity and glucose metabolism in breast cancer stem cells

Project description:Deregulation of Src kinases is associated with cancer. We previously showed that SrcDN conditional expression in MCF7 cells diminished tumorigenesis and causes tumor regression in mice. However, it remained unclear whether SrcDN affected breast cancer stem cell functionality or it reduced tumor mass. Here, we address this question by isolating an enriched population of BCSCs (ESA+-CD44+-CD24-) and the tumor-differentiated cells (ESA+-CD44+-CD24+) from MCF7-Tet-On-SrcDN. ESA+-CD44+-CD24- grew in suspension forming mammospheres, and producing tumors in nude mice, while ESA+-CD44+-CD24+ were poorly/non-tumorigenic. Doxycycline-induction of SrcDN inhibited BCSC tumorigenesis, selfrenewal, and stem-cell markers expression. SrcDN significantly inhibited SFE, and stem-cell markers expression in triple-negative breast cancer (TNBC) MDA-MB-231 and SUM159PT cells. Inducible depletion of c-Src caused similar effects in MDA-MB-231 cells. In MCF7-Tet-On-SrcDN derived mammospheres SrcDN-induction inhibited expression, and activity of hexokinase, pyruvate kinase and lactate dehydrogenase, resulting in diminished glucose consumption and lactate production, which restricted Warburg effect. Thus, c-Src functionality is important for breast cancer stem cell maintenance and renewal, tumorigenicity, and stem cell transcription factor expression, effects linked to glucose metabolism reduction.

2020-07-23 | PXD017789 | Pride

Essential role of miR-200c in regulating self-renewal of breast cancer stem cells initiating from the counter parts of mammary epithelium

Project description:To explore the roles of essential miRNAs in regulating self-renewal of breast cancer stem cells (BCSCs), which initiate from mammary epithelial stem cells (MaSCs). CD44+CD24-/low cells and MUC1-ESA+ cells were isolated by fluorescence-activated cell sorting (FACS) from breast cancer cell line MCF-7 and normal mammary epithelial cell line MCF-10A, and were verified as BCSCs and MaSCs by clonogenic assay and multipotential differentiation experiment in 2-dimensional (2-D) and 3-D cultures, respectively. Using microarray containing oligonucleotides corresponding to 509 miRNAs from human, mouse, and rat genomes. We obtained candidate miRNAs in regulating breast tumorigenesis. One representative miRNA (miR-200c) was proved to regulate stemness of BCSCs and MaSCs in vitro and in vivo by miR-200c agomir transfection. We validated that miR-200c negatively regulated PDCD10, an apoptosis regulator, in BCSCs and MaSCs.

2015-04-26 | GSE68271 | GEO

Differences between CD44+/CD24- and CD44-/CD24+ subpopulation of immortalized human mammary epithelial cells

Project description:CD44+/CD24- subpopulation of normal and cancerous breast epithelial cells are suggested to have stem cell properties. The goal of this study was to identify gene expression differences between CD44+/CD24- and CD44-/CD24+ subpopulation of cells from a same cell lines. We selected MCF-10A cells, which are immortalized derived from a fibrocystic breast disease. These cells are immortalized but not transformed and express basal cell markers. Cells were from a single sort but plated into four 100 mm plates. RNA was prepared from each plate separately for the analysis. Comparison of gene expression between 2 groups ( CD44+/CD24- and CD44-/CD24+) 4 replicates each.

2010-03-07 | E-GEOD-15192 | biostudies-arrayexpress

RUNX transciption factor mediated control of breast cancer stem cells

Project description:Cancer stem cells (CSC) are postulated to be capable of initiating tumor formation, growth, and are resistant to therapies thereby causing tumor recurrence. We flow sorted breast cancer stem cells using CD24 (a negative marker) and CD44 (a positive marker) and performed RNAseq to determine what genes and pathways are altered in the CD24 low/ CD44 high subpopulation relative to CD24high/CD44+ subpopulation.

2020-08-19 | GSE141503 | GEO

Homo sapiens

Project description:miRNA expression profiling in human mammary epithelial cell (HMEC) CD24-CD44+ and non-CD24-CD44+ cell populations

| PRJNA142753 | ENA

Gene expression data from cancer mammospheres and bulk tumors

Project description:Tumorigenic breast cancer cells characterized by CD44 expression and low or undetectable CD24 levels (CD44+/CD24-/low) may be resistant to chemotherapy and therefore responsible for cancer relapse. Paired breast cancer core biopsies before and after neoadjuvant chemotherapy or lapatinib were obtained and as single cell suspensions stained using antibodies against CD24, CD44, and lineage markers, and then analyzed by flow cytometry. Mammosphere (MS) formation in culture was compared before and after treatment. Global gene expression differences between cancer cells bearing CD44+/CD24-/low cells and all other sorted cells, and between cancer MS and the primary bulk invasive cancers were analyzed. We report that CD44+/CD24-/low tumorigenic breast cancer cells were intrinsically chemoresistant ─ chemotherapy led to increased CD44+/CD24-/low cells, increased self-renewal capacity on MS assays, and enhanced tumorigeneicity in immunocompromised SCID/Beige mice. Conversely, in patients with HER2 overexpressing tumors, the EGFR/HER2 tyrosine kinase inhibitor, lapatinib decreased CD44+/CD24-/low cells, with the majority of these patients after conventional therapy achieving pathologic complete response, a validated surrogate marker for long-term survival. Gene transcription pathways that underlie chemoresistant, MS-forming CD44+/CD24-/low cells involve genes belonging to stem cell self-renewal, Wnt signaling, and early development pathways. Keywords: two group comparison

2009-08-15 | GSE7515 | GEO

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