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Gene expression of SUM159 breast cancer cell line expressing microRNA--203

ABSTRACT: Determine the effect of miR-203 expression on the global mRNA expression in mesenchymal breast cancer cell line. Generate control (pBabe puro) and miR-203 (pBabe puro miR-203) cells using retroviral transduction and puromycin selections. Extract total RNA using Trizol.

ORGANISM(S): Homo sapiens

SUBMITTER: Joe Taube

PROVIDER: E-GEOD-50697 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Epigenetic silencing of microRNA-203 is required for EMT and cancer stem cell properties.

Taube Joseph H JH Malouf Gabriel G GG Lu Emily E Sphyris Nathalie N Vijay Vidya V Ramachandran Priyanka P PP Ueno Katumasa R KR Gaur Sanchaika S Nicoloso Milena S MS Rossi Simona S Herschkowitz Jason I JI Rosen Jeffrey M JM Issa Jean-Pierre J JP Calin George A GA Calin George A GA Chang Jeffrey T JT Mani Sendurai A SA

Scientific reports 20130101

The epithelial-mesenchymal transition (EMT) imparts metastatic competence on otherwise non-metastatic cancer cells through decreased inter-cellular adhesions, increased migratory capacity, stem cell properties and anoikis and chemotherapy resistance. In this study, we profiled changes in microRNA expression during EMT in conjunction with changes in DNA methylation at microRNA promoters to discover essential mediators of EMT-imparted stemness properties. MicroRNA-203 (miR-203) expression is repre ...[more]

PMID: 24045437

Similar Datasets

Gene expression of SUM159 breast cancer cell line expressing microRNA--203

Project description:Determine the effect of miR-203 expression on the global mRNA expression in mesenchymal breast cancer cell line.

2013-09-23 | GSE50697 | GEO

MicroRNA-203 represses selection and expansion of oncogenic HRas transformed tumor initiating cells [array]

Project description:In many mouse models of skin cancer, only a few tumors typically form although many cells competent for tumorigenesis receive the same oncogenic mutations. These observations suggest a selection process for defining tumor initiating cells. Here we use quantitative mRNA- and miR-Seq to determine the impact of HRasG12V on the transcriptome of keratinocytes. We discover that microRNA-203 is downregulated by HRasG12V. Using a knockout mouse model, we demonstrate that loss of microRNA-203 promotes selection and expansion of tumor-initiating cells. Conversely, restoration of microRNA-203 with an inducible model potently inhibits proliferation of these cells. We comprehensively identify microRNA-203 targets required for HRas-initiated tumorigenesis. These targets include important effectors of the Ras pathway and essential genes required for cell division. Together, this study establishes a role for the loss of microRNA-203 in promoting selection and expansion of HRas mutated cells and identifies a mechanism through which microRNA-203 antagonizes HRas-mediated tumorigenesis. Identifying mRNA and microRNA networks regulated by oncogenic HRasG12V in primary keratinocytes through the use of 3Seq and small-RNA-Sequencing. Additionally we utilize ribosome-profiling, 3Seq, Microarray and Ago2-HITS-CLIP approaches to identify novel miR-203 target genes.

2015-07-23 | E-GEOD-66055 | biostudies-arrayexpress

Expression data from miR-203 induction in mouse skin

Project description:We identify numerous miR-203 in vivo targets that are highly enriched for the promotion of cell cycle and cell division. Importantly, individual targets including p63, Skp2 and Msi2 play distinct roles downstream of miR-203 to regulate the cell cycle and long-term proliferation. Together, our findings reveal rapid and widespread impact of miR-203 on the self-renewal program during the epidermal differentiation and provide mechanistic insights for the potent role of miR-203 where coordinated repression of multiple targets is required for the function of this miRNA. We used microarrays to measure transcriptome changes upon miR-203's induction in mouse skin and identified new targets of miR-203. We use two pairs of biological duplicates to perform the microarray analysis from the epidermal samples harvested from K14-rtTA/TRE-miR-203/K14-H2BGFP (DP) and TRE-miR-203/K14-H2BGFP (SP) littermates at P4, 24h after the Dox injection.

2013-03-14 | E-GEOD-45121 | biostudies-arrayexpress

Genes regulated by miR-203 in breast cancer cell line MDA-MB-231

Project description:To investigate the mechanism through which miR-203 inhibited the breast cancer cell invasion, we overpression miR-203 in MDA-MB-231 cell line and performed a microarray to examine the genes which maybe targeted and down-regulated by miR-203. We made a stable cell line(MB231/miR-203) which overexpressing miR-203 and a control cell line (MB231/EV) which expressing a contrlol vector. Total RNA were extracted from these two cell lines and subject to microarray.

2013-05-01 | E-GEOD-44239 | biostudies-arrayexpress

Analysis of miR-203 regulated genes during IFNalpha treatment

Project description:The goal of this experiment was to determine gene expression changes during IFNα treatment as the result of expression or inhibition of miR-203 in A549 cells. The gene expression profiling experiment was performed with 4 groups (mock infected, IFNα treated, IFNα treated in the presence of exogenous miR-203, and IFNα treated in the presence of miR-203 inhibitor) with 3 biological replicates for each group. Total RNA was purified from A549 cells that were untreated of treated with IFNα (1000 units/mL) alone or in the presence of miR-203 mimic or inhibitor for 10 hours.

2013-06-20 | E-GEOD-47866 | biostudies-arrayexpress

Expression data from miR-203 induction in mouse skin

2013-03-14 | GSE45121 | GEO

Identification of miR-203 Regulated Genes During Sendai Virus Infection

Project description:The goal of this experiment was to determine gene expression changes during Sendai virus infection as the result of expression or inhibition of miR-203 in A549 cells. The gene expression profiling experiment was performed with 4 groups (mock infected, Sendai virus infected, Sendai virus infeceted in the presence of exogenous miR-203, and Sendai virus infected in the presence of miR-203 inhibitor) with 3 biological replicates for each group. Total RNA was purified from A549 cells that were mock infected or infected with Sendai virus (Cantell strain, 5pfu/cell) alone or in the presence of miR-203 mimic or inhibitor for 10 hours.

2013-06-20 | E-GEOD-47865 | biostudies-arrayexpress

Gene expression analysis in islets from miR-203 TG mice [RNA-seq]

Project description:To investigate the effect of miR-203 in type 2 diabetes, target genes of miR-203 need to be investigated. The β cell specific miR-203 transgene (miR-203 TG) mice was constructed, and RNA-seq was then performed on mouse islets.

2023-05-19 | GSE232473 | GEO

Gene expression analysis in islets from miR-203 TG mice [scRNA-seq]

2023-05-19 | GSE232474 | GEO

IMR90 hTERT

Project description:Transcription profiling from young and pre-senescent IMR90 cells, transfected either with hTERT (pBabe-puro-hTERT) or vector control (pBabe-puro). Population doubling values are contained in Characteristics[generation] column.

2014-06-17 | E-MTAB-2087 | biostudies-arrayexpress

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