RNA-sequencing (RNA-seq) in breast cancer cell lines after ectopic manipulation of miR-26a expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE43726 | GEO | 2016/06/30
SECONDARY ACCESSION(S): PRJNA187476
REPOSITORIES: GEO
Similar Datasets
Project description:RNA sequencing technology has been carried out in order to evaluate mRNA expression changes after manipulation of miR-26a in both MCF-7 and MDA-MB-231 breast cancer cell lines. To evaluate the entire set of genes modulated by miR-26a in breast cancer, we performed RNA-seq after ectopic manipulation of this miRNA. We over-expressed miR-26a in MCF-7 epithelial cancer cell lines and also reduced its activity by stably transfecting MDA-MB-231 mesenchymal-like cancer cell lines with a specific sponge vector. GO terms and pathway enriched analysis of the transcripts that significantly change upon miR-26 ectopic manipulation implicates miR-26ab in cell cycle, apoptosis, cell spreading and cell adhesion in breast cancer
2016-06-30 | E-GEOD-43726 | biostudies-arrayexpress
Project description:RNA sequencing technology has been carried out in order to evaluate mRNA expression changes after manipulation of miR-23b in both MCF-7 and MDA-MB-231 breast cancer cell lines
2013-05-01 | GSE37918 | GEO
Project description:RNA sequencing technology has been carried out in order to evaluate mRNA expression changes after manipulation of miR-23b in both MCF-7 and MDA-MB-231 breast cancer cell lines Our study implicates miR-23b in cytoskeletal remodeling in breast cancer. To evaluate the entire set of genes modulated by miR-23b we performed RNA-seq after ectopic manipulation of this miRNA in breast cancer cell lines. We over-expressed this miRNA in MCF-7 epithelial cancer cell lines and also reduced its activity by stably transfecting MDA-MB-231 mesenchymal-like cancer cell lines with a specific sponge vector. RNA-seq analysis revealed a number of candidate targets of this miRNA.
2013-05-01 | E-GEOD-37918 | biostudies-arrayexpress
Project description:Mesenchymal stromal cells were cultured in 3D PEG hydrogels for 7 days in the presence of serum-free media or conditioned media from a panel of breast cancer cells (MCF-7, MDA-MB-231, MDA-MB-231 lung-tropic, MDA-MB-231 brain-tropic, MDA-MB-231 bone-tropic). In all cases, the secretomes were collected after cancer cells were in serum-free media for 24h.
2019-05-28 | E-MTAB-6998 | biostudies-arrayexpress
Project description:This Series reports results of miRNA profiling of estrogen-receptor-positive (MCF7) and estrogen-receptor-negative (MDA-MB-231) cells. Retinoic Acid (RA) induces mir-21 in MCF-7 but not in MDA-MB-231 cells. MCF-7 and MDA-MB-231 cells were treated (or not) with retinoic acid (RA) and grown for either 6 hours or 48 hours.
2010-05-21 | GSE18628 | GEO
Project description:Objective: Trastuzumab has been used for the treatment of HER2-positive breast cancer (BC). However, a subset of BC patients exhibited resistance to trastuzumab therapy. Thus, clarifying the molecular mechanism of trastuzumab treatment will be beneficial to improve the treatment of HER2-positive BC patients. In this study, we identified trastuzumab-responsive microRNAs that are involved in the therapeutic effects of trastuzumab. Methods and results: RNA samples were obtained from HER2-positive (SKBR3 and BT474) and HER2-negetive (MCF7 and MDA-MB-231) cells with and without trastuzumab treatment for 6 days. Next, we conducted a microRNA profiling analysis using these samples to screen those microRNAs that were up- or downregulated only in HER2-positive cells. This analysis identified miR-26a and miR-30b as trastuzumab-inducible microRNAs. Transfecting miR-26a and miR-30b induced cell growth suppression in the BC cells by 40% and 32%, respectively. A cell cycle analysis showed that these microRNAs induced G1 arrest in HER2-positive BC cells as trastuzumab did. An Annexin-V assay revealed that miR-26a but not miR-30b induced apoptosis in HER2-positive BC cells. Using the prediction algorithms for microRNA targets, we identified cyclin E2 (CCNE2) as a target gene of miR-30b. A luciferase-based reporter assay demonstrated that miR-30b post-transcriptionally reduced 27% (p=0.005) of the gene expression by interacting with two binding sites in the 3’-UTR of CCNE2. Conclusion: In BC cells, trastuzumab modulated the expression of a subset of microRNAs, including miR-26a and miR-30b. The upregulation of miR-30b by trastuzumab may play a biological role in trastuzumab-induced cell growth inhibition by targeting CCNE2. We obtained microRNA expression profiles of breast cancer cell lines, MCF7, MDA-MB-231, SKBR3, and BT474, with or without trastuzumab (4microgram/mL) treatment.
2012-06-02 | E-GEOD-38415 | biostudies-arrayexpress
Project description:The long-term goal of our study is to understand the genetic and epigenetic mechanisms of breast cancer metastasis in human and to discover new possible genetic markers for use in clinical practice. We have used microarray technology (Human OneArray microarray, phylanxbiotech.com) to compare gene expression profiles of non-invasive MCF-7 and invasive MDA-MB-231 cells exposed to dioscin (DS), a steroidal saponin isolated from the roots of wild yam, (Dioscorea villosa). Initially the differential expression of genes (DEG) was identified that followed pathway enrichment analysis (PEA). Of the genes queried on OneArray, we identified 4641 DEG changed between MCF-7 and MDA-MB-231 cells (vehicle-treated) with cut-off log2 |fold change|⧠1. Among these genes, 2439 genes are upregulated and 2002 genes are downregulated. DS exposure (2.30 ïM, 72 h) to these cells identified 801 (MCF-7) and 96 (MDA-MB-231) DEG that showed significant difference compared to untreated cells (p<0.05). Within these gene sets, DS is able to upregulate 395 genes and downregulate 406 genes in MCF-7 and upregulate 36 and downregulate 60 genes in MDA-MB-231 cells. Further comparison of DEG between MCF-7 and MDA-MB-231 cells exposed to DS identified 3626 DEG of which 1700 were upregulated and 1926 genes were down-regulated. From PEA, 12 canonical pathways were significantly altered between these two cell lines (MCF-7 and MDA-MB-231). However, no alteration in any of these pathways was noticed in MCF-7 cell, while in MDA-MB-231 cells only MAPK pathway showed significant alteration. When PEA comparison was made on DS exposed cells, it was observed that only 2 pathways were significantly affected. Further, to identify shared DEG, which are targeted by DS and overlapped in both MCF-7 and MDA-MB-231 cells, we performed intersection analysis (Venn diagram). We found that only 7 DEG are overlapped of which six are reported in the database. This study highlights the diverse gene networks and pathways through which DS exhibits its effect on breast cancer cells. Two condition experiment. Human breast cancer Cell line MCF-7 groups: Vehicle control and dioscin treated; Human breast cancer cell line MDA-MB-231 cell group; vehicle control and dioscin-treated. Biological replicates: MCF-7 control compared to MCF-7 dioscin treated; MDA-MB-231 control compated to MDA-MB-231 dioscin-treated; MCF-7 control compared to MDA-MB-231 control; MCF-7 dioscin treated compared to MDA-MB-231 dioscin-treated. duplicate array
2016-03-22 | E-GEOD-79465 | biostudies-arrayexpress
Project description:RNA-Seq profiling of MCF-7 and MDA-MB-231. We profiled RNA expression in the estrogen-receptor-positive (ER+) MCF-7 and the triple-negative MDA-MB-231 breast cancer cells. The objective was to find genes differentially expressed between these cell lines as potential drivers of invasiveness of the triple-negative MDA-MB-231. We further utilized the identified differential genes to validate expression-responsive module of non-canonical Wnt signaling pathway.
2016-01-21 | GSE73857 | GEO
Project description:This study aimed to further our understanding of the role that CXCR6 plays in breast cancer progression. Microarrays were searched for some genes that had correlated expression with CXCR6 mRNA. According to fold-change screening between restoring expression of CXCR6 and its respective control cells in MDA-MB-231 and MCF-7 cells, both up-regulated and down-regulated genes were shown. The restoring of CXCR6 expression in MDA-MB-231 and MCF-7 cells were respectively noted as MDA-MB-231-CXCR6 and MCF-7-CXCR6 cells and the respective controls were noted as MDA-MB-231-GFP and MCF-7-GFP cells.
2015-06-30 | E-GEOD-60484 | biostudies-arrayexpress
Project description:The long-term goal of our study is to understand the genetic and epigenetic mechanisms of breast cancer metastasis in human and to discover new possible genetic markers for use in clinical practice. We have used microarray technology (Human OneArray microarray, phylanxbiotech.com) to compare gene expression profiles of non-invasive MCF-7 and invasive MDA-MB-231 cells exposed to dioscin (DS), a steroidal saponin isolated from the roots of wild yam, (Dioscorea villosa). Initially the differential expression of genes (DEG) was identified that followed pathway enrichment analysis (PEA). Of the genes queried on OneArray, we identified 4641 DEG changed between MCF-7 and MDA-MB-231 cells (vehicle-treated) with cut-off log2 |fold change|≧ 1. Among these genes, 2439 genes are upregulated and 2002 genes are downregulated. DS exposure (2.30 M, 72 h) to these cells identified 801 (MCF-7) and 96 (MDA-MB-231) DEG that showed significant difference compared to untreated cells (p<0.05). Within these gene sets, DS is able to upregulate 395 genes and downregulate 406 genes in MCF-7 and upregulate 36 and downregulate 60 genes in MDA-MB-231 cells. Further comparison of DEG between MCF-7 and MDA-MB-231 cells exposed to DS identified 3626 DEG of which 1700 were upregulated and 1926 genes were down-regulated. From PEA, 12 canonical pathways were significantly altered between these two cell lines (MCF-7 and MDA-MB-231). However, no alteration in any of these pathways was noticed in MCF-7 cell, while in MDA-MB-231 cells only MAPK pathway showed significant alteration. When PEA comparison was made on DS exposed cells, it was observed that only 2 pathways were significantly affected. Further, to identify shared DEG, which are targeted by DS and overlapped in both MCF-7 and MDA-MB-231 cells, we performed intersection analysis (Venn diagram). We found that only 7 DEG are overlapped of which six are reported in the database. This study highlights the diverse gene networks and pathways through which DS exhibits its effect on breast cancer cells.
2016-03-22 | GSE79465 | GEO