Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-19777
PROVIDER: PRJNA121861 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells
2025-01-24 | E-GEOD-19777 | ExpressionAtlas
Project description:Full title: Expression data from antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells The expression of miR-221/222 were found to be upregulated in fulvestrant resistant breast cancer cells MCF7-FR compared to its drug-sensitive counterpart MCF7. To investigate the role of miR-221/222 in acquired resistance to fulvestrant, we lowered the level of miR-221/222 in MCF7-FR cells using miRNA inhibitors (antagomirs), and compared gene expression profiles before and after treatment.
2011-01-29 | GSE19777 | GEO
Project description:Full title: Expression data from antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells The expression of miR-221/222 were found to be upregulated in fulvestrant resistant breast cancer cells MCF7-FR compared to its drug-sensitive counterpart MCF7. To investigate the role of miR-221/222 in acquired resistance to fulvestrant, we lowered the level of miR-221/222 in MCF7-FR cells using miRNA inhibitors (antagomirs), and compared gene expression profiles before and after treatment. Fulvestrant-resistant breast cancer cells MCF7-FR (originated from drug-sentitive breast cancer model cell line MCF7) were transient-transfected by antigomirs targeting miR221 or miR222 (i.e. si221, si222). All three cell lines, MCF7-FR, siR221, siRNA222 were subjected to gene expression profiling.
2011-01-29 | E-GEOD-19777 | biostudies-arrayexpress
Project description:mRNA breast cancer cell lines were profiled to study the function of hsa-mir-221 and hsa-mir-222. MCF7 cell lines were profiled after treatment with mir-221/222 mimics, and compared to profiles with transfection controls. Similarly, MDA-MB-231 cell lines were profiled after treatment with mir-221/222 inhibitors, and compared to profiles with transfection controls. Since ESR1 is a predicted target of mir-221/222 we also profiled MCF7 cell lines after disrupting ESR1 with an siRNA. Other breast cancer cell lines are provided because all cell lines were normalized together. Keywords: breast cancer, cell line, hsa-mir-221, hsa-mir-222, ESR1
2008-12-01 | GSE10890 | GEO
Project description:Melphalan-induced modulation of miR-221/222 levels in MM cells. Melphalan-resistant U266/LR7 cells showed the highest induction of miR-221/222 after drug exposure. To study the transcriptome perturbation induced in MM cells following the combination of miR-221/222 inhibitors plus melphalan we used the whole gene expression data
2015-09-08 | GSE66618 | GEO
Project description:Melphalan-induced modulation of miR-221/222 levels in MM cells. Melphalan-resistant U266/LR7 cells showed the highest induction of miR-221/222 after drug exposure. To study the transcriptome perturbation induced in MM cells following the combination of miR-221/222 inhibitors plus melphalan we used the whole gene expression data total RNA was obtained after single or combination treatment of the Melphalan-resistant U266/LR7 cells and the parental cell line U266/s
2015-09-08 | E-GEOD-66618 | biostudies-arrayexpress
Project description:mRNA breast cancer cell lines were profiled to study the function of hsa-mir-221 and hsa-mir-222. MCF7 cell lines were profiled after treatment with mir-221/222 mimics, and compared to profiles with transfection controls. Similarly, MDA-MB-231 cell lines were profiled after treatment with mir-221/222 inhibitors, and compared to profiles with transfection controls. Since ESR1 is a predicted target of mir-221/222 we also profiled MCF7 cell lines after disrupting ESR1 with an siRNA. Other breast cancer cell lines are provided because all cell lines were normalized together. Experiment Overall Design: mRNA breast cancer cell line profiles with some samples in duplicate or triplicate. See summary for more information.
2009-01-13 | E-GEOD-10890 | biostudies-arrayexpress
Project description:Macrophages are heterogeneous immune cells with distinct origins, phenotypes, functions and tissue localization. Their susceptibility to HIV-1 is subject to variations from permissiveness to resistance, owing in part to regulatory microRNAs. Here, we used RNAseq to examine the expression of >400 microRNAs in productively infected and bystander cells of HIV-1-exposed macrophage cultures. Two micro-RNAs up regulated in bystander macrophages, miR-221 and miR-222, were identified as negative regulators of CD4 expression and CD4-mediated HIV-1 entry. Both microRNAs were enhanced by TNF-α, an inhibitor of CD4 expression. MiR-221/miR-222 inhibitors recovered HIV-1 entry in TNF-α-treated macrophages by enhancing CD4 expression, and increased HIV-1 replication and spread in macrophages by countering TNF-α-enhanced miR-221/miR-222 expression in bystander cells. In line with these findings, HIV-1-resistant intestinal myeloid cells express higher levels of miR-221 than peripheral blood monocytes. Thus, miR-221/miR-222 act as effectors of the antiviral host response activated during macrophage infection that restrict HIV-1 entry.
2017-09-11 | GSE103394 | GEO
Project description:Gene expression profiling of MCF10A (miR-221/222 vs control)
2025-01-24 | E-GEOD-29327 | ExpressionAtlas
Project description:We profiled miRNA expression in tissue samples (104 HCC, 90 adjacent cirrhotic livers, 21 normal livers) as well as in 35 HCC cell lines. A set of 12 miRNAs (including miR-21, miR-221/222, miR-34a, miR-519a, miR-93,miR-96, and let-7c) was linked to disease progression from normal liver through cirrhosis to full-blown HCC. miR-221/222, the most upregulated miRNAs in tumor samples, are shown to target the CDK inhibitor p27 and to enhance cell growth in vitro. Conversely, these activities can be efficiently inhibited by an antagomiR specific for miR-221. In addition, we show, using a mouse model of liver cancer, that miR-221 overexpression stimulates growth of tumorigenic murine hepatic progenitor cells.
2009-12-08 | E-TABM-866 | biostudies-arrayexpress