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Gene expression patterns induced by 5-Fluorouracil in breast cancer cell lines

ABSTRACT: We have compared the changes in cell cycle and cell death parameters induced by 2 different concentrations of 5-FU (IC50 and IC80) in the breast adenocarcinoma cell line MCF7. G1/S cell cycle arrest was associated with both concentrations, whereas cell death was mainly induced after IC80 5-FU. These changes were correlated with gene expression assessed by cDNA microarray analysis. Main findings included an overexpression of p53 target genes involved in cell cycle and apoptosis (CDKN1A/p21, TP53INP, TNFRSF6/FAS and BBC3/PUMA), and significant repression of Myc. High dose 5-FU also induced a higher regulation of the mitochondrial death genes APAF1, BAK1 and BCL2, and induction of genes of the ID family. Keywords: Dose Response

ORGANISM(S): Homo sapiens

PROVIDER: GSE2584 | GEO | 2006/04/07

SECONDARY ACCESSION(S): PRJNA91993

REPOSITORIES: GEO

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Gene expression patterns induced by 5-Fluorouracil in breast cancer cell lines

Project description:We have compared the changes in cell cycle and cell death parameters induced by 2 different concentrations of 5-FU (IC50 and IC80) in the breast adenocarcinoma cell line MCF7. G1/S cell cycle arrest was associated with both concentrations, whereas cell death was mainly induced after IC80 5-FU. These changes were correlated with gene expression assessed by cDNA microarray analysis. Main findings included an overexpression of p53 target genes involved in cell cycle and apoptosis (CDKN1A/p21, TP53INP, TNFRSF6/FAS and BBC3/PUMA), and significant repression of Myc. High dose 5-FU also induced a higher regulation of the mitochondrial death genes APAF1, BAK1 and BCL2, and induction of genes of the ID family. Time and dose-dependent changes in gene expression, induced by 5-Fluorouracil, in breast carcinoma cell lines MCF7, and MDA-MB-435.

2010-07-01 | E-GEOD-2584 | biostudies-arrayexpress

Mouse models to investigate in situ cell fate decisions induced by TP53 and other factors (CUT&RUN)

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Interactome of Arabidopsis BIR3 protein

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Sca1+ macrophages activate hematopoietic stem/progenitor cells upon bone marrow stress. [scRNA-Seq]

Project description:Although hematopoietic stem and progenitor cells (HSPCs) become activated in the cell-cycle status after chemotherapy to supply hematopoietic loss, the detailed mechanisms of activation remain unknown. Here we show that Sca1+ macrophages play a key role for bone marrow (BM) recovery through granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion. By analyzing gene expression profiles of HSPCs lodged in 5-fluolouracil (5-FU)-treated mice, we found GM-CSF as a key proliferative signal. Sca1+ macrophages in BM after 5-FU treatment expressed high levels of GM-CSF. GM-CSF-knockout mice treated with 5-FU were lethal because of severe BM suppression. Up-regulation of Csf2 in Sca1+ macrophages by 5-FU was suppressed in MyD88-knockout mice, suggesting that TLR signaling via damage-associated molecular patterns caused by cell death is critical for up-regulation of Csf2. In 5-FU treated BM, majority of Sca1+ macrophages and transplanted HSPCs locate perivascular areas. These findings together indicate that Sca1+ macrophages induce HSPCs to proliferate through GM-CSF signaling in the stressed BM environments.

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Sca1+ macrophages activate hematopoietic stem/progenitor cells upon bone marrow stress. [RNA-Seq]

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Transcription profiling of non-small cell lung carcinoma cell line H1975 treated with cisplatin or BMS-69014 a novel panHER/VEGFR inhibitor

Project description:Non-small cell lung cancer (NSCLC) with activating mutations in the epidermal growth factor receptor (EGFR) responds to EGFR tyrosine kinase inhibitors such as erlotinib. However, secondary somatic EGFR mutations (e.g. T790M) confer resistance to erlotinib. BMS-690514, a novel panHER/VEGFR inhibitor described here, exerted antiproliferative and pro-apoptotic effects on NSCLC cell lines, with prominent efficacy on H1975 cells expressing the T790M mutation. In this model, BMS-690514 induced a G1 cell cycle arrest, as well as ultrastructural hallmarks of apoptosis, mitochondrial release of cytochrome c, and activation of caspases involved in the intrinsic (e.g. caspase -2, -3, -7 and -9), but not in the extrinsic (e.g. caspase-8) pathway. Caspase inhibition conferred partial protection against BMS-690514 cytotoxicity, pointing to the involvement of both caspase-dependent and -independent effector mechanisms. Transcriptome analyses revealed the upregulation of pro-apoptotic (e.g. Bim, Puma) and cell cycle inhibitory (e.g. p27Kip1, p57Kip2) factors, as well as the downregulation of anti-apoptotic (e.g. Mcl1), heat shock (e.g. HSP40, HSP70, HSP90) and cell cycle promoting (e.g. cyclins B1, D1 and D3, CDK1, MCM family proteins, PCNA) proteins. BMS-690514-induced death of H1975 cells was modified in a unique fashion by a panel of siRNAs targeting apoptosis modulators. Downregulation of components of the NF-kappaB survival pathway (e.g. p65, Nemo/IKK, TAB2) sensitized cells to BMS-690514, whereas knockdown of pro-apoptotic factors (e.g. Puma, Bax, Bak, caspase-2, etc) and DNA damage-related proteins (e.g. ERCC1, hTERT) exerted cytoprotective effects. BMS-690514 is a new pan-HER/VEGFR inhibitor that may become an alternative to erlotinib for the treatment of NSCLC.

2007-07-24 | E-TABM-239 | biostudies-arrayexpress

Arabidopsis thaliana

Project description:Specific control of Arabidopsis BAK1- and SERK4-regulated cell death by protein glycosylation

| PRJNA294262 | ENA

New insights into the molecular mechanisms of 1,3-dinitrobenzene-induced testicular toxicity

Project description:Several studies have shown that 1,3-dinitrobenzene (DNB) causes injury to Sertoli cells and induces apoptosis in the surrounding germinal cells in male laboratory rats ; however, the mechanisms by which DNB functions are not well understood. In this context, we have conducted studies using standard parameters and molecular tools to better understand the pathogenesis of the testicular effects produced by DNB, as well as its mode of action. Wistar rats were orally exposed to 0.1-8 mg DNB/kg/day for 4 days. Testosterone concentrations were not affected at any dose level, but marked histopathological lesions in the testes were recorded at 4 mg/kg/day. Global transcriptomic analysis of rat testes revealed cell cycle and cell death as the major biological processes affected. In particular, we identified an alteration in the expression of genes associated with cell cycle progression (mitotic roles of polo-like kinase). Dinitrobenzene was administered in suspension to rats (7 weeks old at start of treatment) by oral gavage at a daily dose of 0 (control, 0.5% methylcellulose in sterilized water), 0.1, 1, and 4 mg/kg body weight, for 4 consecutive days. Dose-related changes in gene expression were determined in the testes using whole genome oligonucleotide microarrays.

2012-07-13 | E-GEOD-39344 | biostudies-arrayexpress

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