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RNA sequencing analysis of wild-type and BML-210 treated breast cancer EO771

ABSTRACT: RNA sequencing analysis of wild-type and BML-210 treated breast cancer EO771

PROVIDER: PRJNA758421 | ENA |

REPOSITORIES: ENA

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RNA sequencing analysis of wild-type and BML-210 treated breast cancer EO771

Project description:We investigated the molecular mechanism by which BML-210 enhanced the response of breast tumor cells to cytotoxic CD8+ T cells. For this purpose, we performed RNA sequencing and analyzed the genome-wide gene expression profiles to systematically identify transcriptom reprogramming in the BML-210-treated cells.

2021-10-04 | GSE182954 | GEO

Transcriptome profiling of brown adipocytes treated with BML-260, DMSO or ISO for revealing the BML-260 mechanism

Project description:To explore BML-260 how to increase thermogenesis, we treated brown adipocytes with BML-260 and DMSO for 1 day or 3 days after seven days' differenciation. Meanwhile, we also set ISO (isoproterenol)-treated brown adipocytes as positive control. We found that BML-260 treatment led to very significant upregulation of genes involved in oxidative phosphorylation, fatty acid beta-oxidation, and mitochondrial function.When compared to cells treated with ISO, although both showed significant upregulation of UCP1, BML-260-treated cells showed a rather distinct gene profile when compared to ISO-treated cells. This work provides evidences that BML-260 can also exert a JSP-1-independent effect in activating UCP1 and thermogenesis in adipocytes, and be potentially applied to treat obesity.

2019-04-16 | GSE129791 | GEO

Transcriptome profiling of mouse subcutaneous white adipose tissue treated with BML-260

Project description:To explore BML-260 how to increase thermogenesis, we examined the effect of BML-260 by direct in situ injection into the subcutaneous white adipose depot. Three days after a single injection, mice were dissected and subcutaneous adipose tissues were obtained for RNA extraction. we noticed that BML-260 treatment resulted in a very significant upregulation of genes involved in thermogenesis. And gene signatures of muscle cell differentiation, muscle structure development, regulation of muscle system process were among the most enriched GO terms. Our work provides evidences that BML-260 can also exert a JSP-1-independent effect in activating UCP1 and thermogenesis in adipocytes, and be potentially applied to treat obesity.

2019-04-14 | GSE129771 | GEO

BML

Project description:bml SEQ

| PRJEB33313 | ENA

Functional analyses of miR-210 involvement in the aggressive phenotype of high grade breast tumors

Project description:As miR-210 expression is correlated to poor prognosis both in estrogen-positive and in estrogen-negative breast cancer (BC) patients, we aimed to investigate the biological processes regulated by miR-210 and which may elucidate its function in the aggressive phenotype of high grade breast cancer. We performed in silico functional analyses of the genes deregulated upon miR-210 overexpression in MCF7 BC cell line and upon miR-210 repression in MDA-MB-231 BC cell line using lentiviral transduction. Gene expression profiling analysis of these cells revealed the deregulation of genes involved in several biological pathways including cell adhesion, extracellular structure organization, epithelial cell proliferation, cell division, cell cycle and immune response.

2011-07-01 | GSE25162 | GEO

Functional analyses of miR-210 involvement in the aggressive phenotype of high grade breast tumors

2011-07-01 | E-GEOD-25162 | biostudies-arrayexpress

Transcriptome profiling of brown adipocytes treated with BML-260, DMSO or ISO for revealing the BML-260 mechanism

Project description:Transcriptome profiling of brown adipocytes treated with BML-260, DMSO or ISO for revealing the BML-260 mechanism

| PRJNA532837 | ENA

MiR-210 is induced by Oct-2, regulates B-cells and inhibits autoantibody production

Project description:MicroRNAs are small, non-coding RNAs that regulate gene expression post-transcriptionally. Here, we show that miR-210 is induced by Oct-2, a key transcriptional mediator of B-cell activation. Germline deletion of miR-210 results in the development of autoantibodies from 5 months of age. Overexpression of miR-210 in vivo resulted in cell autonomous expansion of the B1 lineage and impaired fitness of B2 cells. Mice over-expressing miR-210 exhibited impaired class-switched antibody responses, a finding confirmed in wild-type B-cells transfected with a miR-210 mimic. In vitro studies demonstrated a defect in cellular proliferation and cell-cycle entry, which was consistent with the transcriptomic analysis demonstrating down-regulation of genes involved in cellular proliferation and B cell activation. These findings indicate that Oct-2 induction of miR-210 provides a novel inhibitory mechanism for the control of B cells and autoantibody production.

2013-06-21 | GSE48186 | GEO

Nostoc sp. MBR 210 isolate:MBR 210

Project description:Nostoc sp. MBR 210 isolate:MBR 210 Genome sequencing and assembly

| PRJNA329640 | ENA

Mouse miR-210 activity in B-cells

Project description:mRNA profiling of miR-210 transgenic (in vivo), mimic-transfected (in vitro) and miR-210 knockout activated mouse B-cells was performed to assess the effect of miR-210 overexpression on the B-cell transcriptome.

2013-08-23 | E-MTAB-1758 | biostudies-arrayexpress

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