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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse Stat3flx/flx/NIC breast tumors compared to wild type NIC tumors

ABSTRACT: A Stat3-dependent transcription regulatory network involved in inflammation and metastasis is identified. Analyses of the gene expression data revealed that Stat3flx/flx/NIC tumors exhibited a significant reduction in the expression of factors involved in both tumor angiogenesis (fibronectin, von willebrand factor, annexin a3, thrombopoietin, fibulin 5) and in the acute phase inflammatory response (cebpd, osmr, saa1, saa2) Experiment Overall Design: Common reference design. 8 samples including RNA extracted from 3 pools of Stat3wt/wt/NIC (WT) tumor tissues (5 individual tumor samples per pool) and 5 individual Stat3flx/flx/NIC (Homo) tumor tissue samples.

ORGANISM(S): Mus musculus

SUBMITTER: Solmaz Shahalizadeh

PROVIDER: E-GEOD-15632 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Identification of a Stat3-dependent transcription regulatory network involved in metastatic progression.

Ranger Jill J JJ Levy David E DE Shahalizadeh Solmaz S Hallett Michael M Muller William J WJ

Cancer research 20090818 17

High levels of activated Stat3 are often found in human breast cancers and can correlate with poor patient outcome. We employed an activated ErbB2 mouse model of breast cancer to investigate the in vivo role of Stat3 in mammary tumor progression and found that Stat3 does not alter mammary tumor initiation but dramatically affects metastatic progression. Four-fold fewer animals exhibited lung metastases in the absence of Stat3 and a 12-fold reduction in the number of lung lesions was observed in ...[more]

PMID: 19690134

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Gene expression profiling of Stat3flx/flx/NIC breast tumors compared to wild type NIC tumors.

Project description:A Stat3-dependent transcription regulatory network involved in inflammation and metastasis is identified. Analyses of the gene expression data revealed that Stat3flx/flx/NIC tumors exhibited a significant reduction in the expression of factors involved in both tumor angiogenesis (fibronectin, von willebrand factor, annexin a3, thrombopoietin, fibulin 5) and in the acute phase inflammatory response (cebpd, osmr, saa1, saa2)

2009-09-01 | GSE15632 | GEO

Mus musculus strain:FVB

Project description:Transcriptome analysis of NIC+DOCK1wt/wt and NIC+DOCK1flx/flx mice mammary tumors

| PRJNA189677 | ENA

Mus musculus

Project description:Gene expression profiling of Stat3flx/flx/NIC breast tumors compared to wild type NIC tumors.

| PRJNA115629 | ENA

JNK pathway blockade promotes HER2-driven breast cancer [RNA-seq_primary_mammary_tumor_cell_lines]

Project description:JNK deletion in MMTV-NIC mouse model promotes mammary gland tumor formation.

2022-12-21 | GSE200521 | GEO

EGFRvIII/STAT3 targets in glioblastoma pathogenesis

Project description:Next generation sequencing platforms were used to identify STAT3 targets in the background of EGFRvIII expresssion mRNA of 3 EGFRvIII positive brain tumor stem cell lines (BTSC #68, 73, and 90) were compared to an EGFRvIII negative line (#41) to identify EGFRvIII-regulated targets in human BTSC. EGFRvIII-dependent targets in mouse astrocytes were identified by mRNA-seq analyses of EGFRvIII- or MSCV-expressing astrocytes. STAT3-differentially regulated genes in EGFRvIII expressing mouse astrocytes were obtained by subjecting EGFRvIII,STAT3f/f and EGFRvIII, STAT3-/- astrocytes to mRNA-Seq analyses. Sites of STAT3 occupancy in EGFRvIII expressing astrocytes were identified by ChIP-Seq using a STAT3 antibody or IgG control. We identified OSMR as a direct target of STAT3 in both EGFRvIII-expressing human BTSC and mouse astrocytes. Therefore to identify OSMR-regulated genes, we used a lentiviral mediated RNAi system to knockdown OSMR in EGFRvIII-expressing astrocytes. OSMR-dependent differentially expressed genes were obtained by comparison of OSMR knockdown (KD1 and KD2) astrocytes to control groups (ShRNA control and Vector control)

2016-04-13 | E-GEOD-51281 | biostudies-arrayexpress

Transcription profiling of PTEN-deficiency in luminal MMTV-ErbB-2 mouse model to investigate its effect on mammary tumorigenesis and metastasis

Project description:Overexpression and/or amplification of the ErbB-2 oncogene, as well as inactivation of the tumor suppressor PTEN, are two important genetic events in human breast carcinogenesis. To address the biological impact of conditional inactivation of PTEN on ErbB-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the MMTV promoter to directly couple expression of activated ErbB-2 and Cre recombinase to the same mammary epithelial cell (MMTV-NIC). Disruption of PTEN in the mammary epithelium of the MMTV-NIC model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology. PTEN-deficient/NIC tumorigenesis was associated with an increase in angiogenesis. Moreover, inactivation of PTEN in the MMTV-NIC mouse model resulted in hyperactivation of the PI3K/Akt signalling pathway. However, like the parental strain, tumors obtained from PTEN-deficient/NIC mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer. Taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by PTEN deficiency and ErbB-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways. Experiment Overall Design: Common reference design. 9 samples (including 2 normal tissue and 7 tumor tissue samples) replicated twice as dye swaps, generating a total of 18 arrays.

2009-07-03 | E-GEOD-13916 | biostudies-arrayexpress

Distinct oncogenic roles of protein arginine methyltransferases (PRMTs) in mammary gland tumorigenesis using transgenic overexpression mouse models

Project description:DEGs in the mammary epithelical cells between NIC and NIC-Prmt

2020-04-01 | GSE111624 | GEO

PTEN-deficiency in luminal MMTV-ErbB-2 mouse model results in dramatic acceleration in mammary tumorigenesis/metastasis

2009-06-29 | GSE13916 | GEO

Effects of SAA treatment on global gene expression in THP-1 derived macrophages

Project description:The effect of SAA1 treatment on global gene expression in THP-1 macrophages was studied. The study determined the gene expression upon wild-type SAA1 treatment, variant SAA1 treatment (p.Gly72Asp) and in untreated THP-1 macrophages. SAA1 treatment of macrophages induces the expression of genes involved in inflammation, angiogenesis, phagocytosis and tissue remodeling which are important in the pathogenesis of chronic inflammatory diseases such as atherosclerosis and rheumatoid arthritis. THP-1 macrophages were treated with SAA1 for either 8 hours or 24 hours. RNA were then extracted and the gene expression pattern was compared between (i) wild-type SAA1 vs untreated (ii) variant SAA1 vs wild-type SAA1 at both 8 hr and 24 hr.

2011-05-11 | E-GEOD-28785 | biostudies-arrayexpress

SAA1-dependent reprogramming of adipocytes by tumor cells is associated with triple negative breast cancer aggressiveness

Project description:Cancer development and progression depend on tumor cell intrinsic factors, the tumor microenvironment and host characteristics. Despite the identification of the plasticity of adipocytes, the primary breast stromal cells, both in physiology and cancer, we lack a complete understanding of mechanisms that regulate adipocyte-tumor cell crosstalk. Here we dissected the breast cancer crosstalk with adipocytes and studied relevant molecules. We identified that the ability of breast cancer cells to dedifferentiate adipocytes is intrinsic subtype-dependent, with all breast cancer subtypes, except for HER2+ER+ subtype, capable of inducing this phenomenon. Crosstalk between breast cancer cells and adipocytes in vitro increased cancer stem-like features and recruitment of pro-tumorigenic immune cells, through chemokine production. Serum amyloid A1 (SAA1) was in vitro identified as a regulator of the adipocyte dedifferentiation program in triple-negative breast cancer (TNBC) through CD36 and P2XR7 signaling. In human TNBCs, SAA1 expression was associated with CAA infiltration, inflammation, stimulated lipolysis, stem-like properties and distinct tumor immune microenvironment. Our findings provide evidence that interaction between tumor cells and adipocytes through SAA1 release is relevant to the aggressiveness of TNBC, potentially supporting its targeting.

2024-01-15 | PXD041186 | Pride

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