Gene expression of SUM159-mir100 ALDH+ and ALDH- cells from CTRL or mir100-overexpressing group
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE59361 | GEO | 2014/12/04
SECONDARY ACCESSION(S): PRJNA255137
REPOSITORIES: GEO
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Project description:Emerging evidence suggest that miRNAs play an essential role in self-renewal and differentiation of normal and malignant stem cells by regulating the expression of key stem cell regulatory genes. Here we demonstrate that mir-100 expression is related to cellular differentiation state with lowest expression in cells displaying stem cell markers. Utilizing a tetracycline inducible lentivirus driving mir-100 expression, we found that mir-100 overexpression decreased breast cancer stem cells (BCSCs) and inhibited cancer cell proliferation in vitro and in mouse xenografts by targeting SMARCA5, SMARCD1 and BMPR2. In order to determine the cellular targets of mir-100 in BCSCs and non-BCSCs, ALDH-positive and -negative populations of pTRIPZ-SUM159-mir-100 cells were separated and cultured in suspension for ten hours in the presence or absence of DOX. Gene expression profiles of the four populations were determined utilizing Affymetrix microarrays
2014-12-04 | E-GEOD-59361 | biostudies-arrayexpress
Project description: Not available
| S-ECPF-GEOD-59361 | biostudies-other
Project description:It has been suggested that breast cancers are driven and maintained by a cellular subpopulation with stem cell properties. These breast cancer stem cells (BCSCs) mediate metastasis and by virtue of their resistance to radiation and chemotherapy, contribute to relapse. Although several BCSC markers have been described, it is unclear whether these markers identify the same or independent BCSC populations. Based on established breast cancer cell lines, as well as primary tumor samples and xenografts, we show that BCSCs exist in distinct mesenchymal-like (epithelial-mesenchymal transition, EMT) and epithelial-like (mesenchymal-epithelial transition, MET) states characterized by expression of distinct markers, proliferative capacity and invasive characteristics. The gene expression profiles of mesenchymal-like and epithelial-like BCSCs are remarkably similar across the different molecular subtypes of breast cancer and resemble those of distinct basal and luminal stem cells found in the normal breast. We propose that the plasticity of BCSCs allowing them to transition between EMT- and MET-like states endows these cells with the capacity for tissue invasion, dissemination and growth at metastatic sites. Breast cancer cells from patient were sorted using flow cytometry to select for cells that were ALDH+. Gene expression profiles of these cells were compared with profiles of ALDH- cells.
2013-11-14 | E-GEOD-52327 | biostudies-arrayexpress
Project description:It has been suggested that breast cancers are driven and maintained by a cellular subpopulation with stem cell properties. These breast cancer stem cells (BCSCs) mediate metastasis and by virtue of their resistance to radiation and chemotherapy, contribute to relapse. Although several BCSC markers have been described, it is unclear whether these markers identify the same or independent BCSC populations. Based on established breast cancer cell lines, as well as primary tumor samples and xenografts, we show that BCSCs exist in distinct mesenchymal-like (epithelial-mesenchymal transition, EMT) and epithelial-like (mesenchymal-epithelial transition, MET) states characterized by expression of distinct markers, proliferative capacity and invasive characteristics. The gene expression profiles of mesenchymal-like and epithelial-like BCSCs are remarkably similar across the different molecular subtypes of breast cancer and resemble those of distinct basal and luminal stem cells found in the normal breast. We propose that the plasticity of BCSCs allowing them to transition between EMT- and MET-like states endows these cells with the capacity for tissue invasion, dissemination and growth at metastatic sites.
2013-11-14 | GSE52327 | GEO
Project description:It has been suggested that breast cancers are driven and maintained by a cellular subpopulation with stem cell properties. These breast cancer stem cells (BCSCs) mediate metastasis and by virtue of their resistance to radiation and chemotherapy, contribute to relapse. Although several BCSC markers have been described, it is unclear whether these markers identify the same or independent BCSC populations. Based on established breast cancer cell lines, as well as primary tumor xenografts, we show that BCSCs exist in distinct mesenchymal-like (epithelial-mesenchymal transition, EMT) and epithelial-like (mesenchymal-epithelial transition, MET) states characterized by expression of distinct markers, proliferative capacity and invasive characteristics. The gene expression profiles of mesenchymal-like and epithelial-like BCSCs are remarkably similar across the different molecular subtypes of breast cancer and resemble those of distinct basal and luminal stem cells found in the normal breast. We propose that the plasticity of BCSCs allowing them to transition between EMT- and MET-like states endows these cells with the capacity for tissue invasion, dissemination and growth at metastatic sites. Breast cancer cell lines, primary xenografts and normal breast cells from patient were sorted using flow cytometry to select for cells that were CD24-,CD44+ and ALDH+. Gene expression profiles of CD24-CD44+ cells were compared with non-CD24-CD44+ cells. Gene expression profiles of ALDH+ cells were compared with ALDH- cells.
2013-11-13 | E-GEOD-52262 | biostudies-arrayexpress
Project description:It has been suggested that breast cancers are driven and maintained by a cellular subpopulation with stem cell properties. These breast cancer stem cells (BCSCs) mediate metastasis and by virtue of their resistance to radiation and chemotherapy, contribute to relapse. Although several BCSC markers have been described, it is unclear whether these markers identify the same or independent BCSC populations. Based on established breast cancer cell lines, as well as primary tumor xenografts, we show that BCSCs exist in distinct mesenchymal-like (epithelial-mesenchymal transition, EMT) and epithelial-like (mesenchymal-epithelial transition, MET) states characterized by expression of distinct markers, proliferative capacity and invasive characteristics. The gene expression profiles of mesenchymal-like and epithelial-like BCSCs are remarkably similar across the different molecular subtypes of breast cancer and resemble those of distinct basal and luminal stem cells found in the normal breast. We propose that the plasticity of BCSCs allowing them to transition between EMT- and MET-like states endows these cells with the capacity for tissue invasion, dissemination and growth at metastatic sites.
2013-11-13 | GSE52262 | GEO
Project description:MicroRNAs (miRNAs) have been globally profiled in cancers but there tends to be poor agreement between studies including in the same cancers. Additionally, few putative miRNA targets have been validated. To overcome the lack of reproducibility, we profiled miRNAs by next generation sequencing and locked nucleic acid miRNA microarrays, and we verified concordant changes by quantitative RT-PCR. Notably, miR-125b and the miR-99 family members miR-99a, -99b, -100 were down-regulated in all assays in advanced prostate cancer cell lines relative to the parental cell lines from which they were derived. All four miRNAs were also down-regulated in human prostate tumor tissue compared to normal prostate. Transfection of miR-99a, -99b or -100 inhibited the growth of prostate cancer cells and decreased the expression of prostate-specific antigen (PSA), suggesting potential roles as tumor suppressors in this setting. To identify targets of these miRNAs, we combined computational prediction of potential targets with experimental validation by microarray and polyribosomal loading analysis. Three direct targets of the miR-99 family that were validated in this manner were the chromatin remodeling factors SMARCA5 and SMARCD1 and the growth regulatory kinase mTOR. We determined that PSA is post-transcriptionally regulated by the miR-99 family members at least partially by repression of SMARCA5. Together, our findings suggest key functions and targets of miR-99 family members in prostate cancer suppression and prognosis. C4-2 cells were transfected with miR-99a and harvested after 48hr. si-GL2 was used as control.
2010-12-29 | E-GEOD-26332 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) have been globally profiled in cancers but there tends to be poor agreement between studies including in the same cancers. Additionally, few putative miRNA targets have been validated. To overcome the lack of reproducibility, we profiled miRNAs by next generation sequencing and locked nucleic acid miRNA microarrays, and we verified concordant changes by quantitative RT-PCR. Notably, miR-125b and the miR-99 family members miR-99a, -99b, -100 were down-regulated in all assays in advanced prostate cancer cell lines relative to the parental cell lines from which they were derived. All four miRNAs were also down-regulated in human prostate tumor tissue compared to normal prostate. Transfection of miR-99a, -99b or -100 inhibited the growth of prostate cancer cells and decreased the expression of prostate-specific antigen (PSA), suggesting potential roles as tumor suppressors in this setting. To identify targets of these miRNAs, we combined computational prediction of potential targets with experimental validation by microarray and polyribosomal loading analysis. Three direct targets of the miR-99 family that were validated in this manner were the chromatin remodeling factors SMARCA5 and SMARCD1 and the growth regulatory kinase mTOR. We determined that PSA is post-transcriptionally regulated by the miR-99 family members at least partially by repression of SMARCA5. Together, our findings suggest key functions and targets of miR-99 family members in prostate cancer suppression and prognosis.
2010-12-29 | GSE26332 | GEO
Project description:Accumulating evidence suggests that microRNAs play definite roles in the pathogenesis of endometriosis. The objective of the study was to determine the role of miR-100-5p, one of the upregulated microRNA in endometriotic cyst stromal cells, in the pathogenesis of endometriosis. Downstream targets of miR-100-5p were identified by compulsory expression of miR-100-5p in normal eutopic endometrial stromal cells (NESCs), a global mRNA microarray technique, and pathways analysis.Compulsory expression of miR-100-5p in NESCs directed the induction of cell motility through SWItch/sucrose non-fermentable (SWI/SNF)-related matrix-associated actin-dependent regulator of chromatin subfamily D member 1 (SMARCD1) supression and matrix metallopeptidase 1 (MMP1) activation.
2020-04-22 | GSE139954 | GEO
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