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Expression data from cultured primary mouse dermal fibroblasts

ABSTRACT: In previous investigations, we detected that growth of melanoma cells in mice depleted for adam9 is enhanced. This resulted from molecular alterations in stromal cells cross-communicating to tumor cells and from constitutively altered expression of some molecules, e.g., TIMP1 in stromal fibroblasts lacking adam9. We used microarray analysis to identify the gene expression alterations occurring in stromal cells upon adam9 deletion which lead to the molecular alterations observed and contribute to the tumor phenotype. Primary fibroblasts from adam9 KO and WT mice were cultured in standard conditions to address constitutive gene alterations.

ORGANISM(S): Mus musculus

SUBMITTER: Yongde Bao

PROVIDER: E-GEOD-56304 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from cultured primary mouse dermal fibroblasts

Project description:In previous investigations, we detected that growth of melanoma cells in mice depleted for adam9 is enhanced. This resulted from molecular alterations in stromal cells cross-communicating to tumor cells and from constitutively altered expression of some molecules, e.g., TIMP1 in stromal fibroblasts lacking adam9. We used microarray analysis to identify the gene expression alterations occurring in stromal cells upon adam9 deletion which lead to the molecular alterations observed and contribute to the tumor phenotype.

2014-03-28 | GSE56304 | GEO

Severe infection constitutively upregulates TIMP1 in the bone marrow hematopoietic niche to support long-term enhanced myelopoiesis

Project description:Infection is able to elicit innate immunological memory by enhancing a long-term myeloid output even after the inciting infectious agent has been cleared. However, mechanisms underlying such a regulation are not fully understood. Using a mouse polymicrobial peritonitis (sepsis) model, we show that severe infection leads to increased, sustained myelopoiesis after the infection is resolved. The infection experience is imprinted in the bone marrow (BM) stromal cells, in the form of a constitutive upregulation of the tissue inhibitor of metalloproteinases 1 (TIMP1). TIMP1 antagonizes the function of ADAM10, an essential cleavage enzyme for the activation of Notch which in turn suppresses myelopoiesis. While TIMP1 is dispensable for myelopoiesis under the steady state, increased TIMP1 enhances myelopoiesis post infection. Thus, our data reveal that infection could establish an inflammatory memory in the BM niche to support a long-term enhanced output of innate immune cells.

2022-06-15 | GSE205728 | GEO

CD99 is a novel prognostic stromal marker in non-small cell lung cancer

Project description:The delicate interaction between cancer cells and the surrounding stroma plays an essential role in all stages of tumourigenesis. Despite the significance of this interplay, alterations in protein composition underlying tumour-stroma interactions are largely unknown. The aim of this study was to identify stromal proteins with clinical relevance in non-small cell lung cancer. A list encompassing 203 stromal candidate genes was compiled based on gene expression array data and available literature. The protein expression of these genes in human NSCLC was screened utilising the Human Protein Atlas. Twelve proteins were selected that showed a differential stromal staining pattern. The corresponding antibodies were applied on a tissue microarray, including 190 NSCLC samples, and stromal staining was correlated with clinical parameters. Higher stromal expression of CD99was associated with good prognosis in the univariate (p=0.037) and multivariate (p=0.039) analyses. The association was independent from the total proportion of tumour stroma, the fraction of inflammatory cells, and clinical and pathological parameters like stage, performance status and tumour histology. The prognostic impact of stromal CD99 protein expression was confirmed in an independent cohort of 240 NSCLC patients (p=0.008). Furthermore, double-staining confocal fluorescence microscopy showed that CD99 was expressed in stromal lymphocytes as well as in cancer associated fibroblasts. Based on a comprehensive screening strategy the membrane protein CD99 was identified as a novel stromal factor with clinical relevance. The result supports the concept that stromal properties have a significant impact on tumourigenesis. Tissue from five tumors were compared to corressponding microdissected tissue from the same tissue sample

2012-06-05 | E-GEOD-33363 | biostudies-arrayexpress

Comparisons of transcriptome among several human iPSC clones derived from different origin and different donors

Project description:Genetically matched human iPSCs from different origins were generated using bone marrow stromal cells and dermal fibroblasts of the same donor, and the global gene expression profile were analyzed. Comparison of gene expressions among 14 iPS clones, 4 and 4 were derived from bone marrow stromal cells(BM), 2 and 4 were from dermal skin fibroblasts(SF) of donor90 and 91, respectively.

2013-01-01 | E-GEOD-41202 | biostudies-arrayexpress

TIMP1 overexpression mediates resistance of MCF-7 human breast cancer cells to fulvestrant and down-regulates progesterone receptor expression

Project description:High levels of Tissue Inhibitor of Metalloproteinases-1 (TIMP1) are associated with poor prognosis, reduced response to chemotherapy, and, potentially, also poor response to endocrine therapy in breast cancer patients. Our objective was to further investigate the hypothesis that TIMP1 is associated with endocrine sensitivity. We established a panel of 11 MCF-7 subclones with a wide range of TIMP1 mRNA and protein expression levels. Cells with high expression of TIMP1 versus low TIMP1 displayed significantly reduced sensitivity to the antiestrogen fulvestrant (ICI 182,780, FaslodexÂ®), while TIMP1 levels did not influence the sensitivity to 4-hydroxytamoxifen. An inverse correlation between expression of the progesterone receptor and TIMP1 was found, but TIMP1 levels did not correlate with estrogen receptor levels or growth-promoting effects of estrogen (estradiol, E2). Additionally, the effects of fulvestrant, 4-hydroxytamoxifen, or estrogen on estrogen receptor expression were not associated with TIMP1 levels. Gene expression analyses revealed associations between expression of TIMP1 and genes involved in metabolic pathways, epidermal growth factor receptor 1/cancer signaling pathways, and cell cycle. Gene and protein expression analyses showed no general defects in estrogen receptor signaling except from lack of progesterone receptor expression and estrogen inducibility in clones with high TIMP1. The present study suggests a relation between high expression level of TIMP1 and loss of progesterone receptor expression combined with fulvestrant resistance. Our findings in vitro may have clinical implications as the data suggest that high tumor levels of TIMP1 may be a predictive biomarker for reduced response to fulvestrant. Microarray analysis of total RNA from 10 subclones of MCF-7 breast cancer cells with various expression levels of TIMP1.

2013-08-22 | E-GEOD-35535 | biostudies-arrayexpress

Expression profile of stromal cells in the lymph node

Project description:Tissue structure of the lymph node (LN) is supported by the network of stromal cells of mesenchymal origin, which is suggested to contribute to various immunological processes. In order to identify stromal cellM-bM-^@M-^Sderived factors that regulate immune function, we performed gene expression profiling of stromal cells freshly isolated from collagenase digested mouse LNs, cultured stromal cell lines, and embryonic fibroblasts as a mesenchymal control. Total RNAs extracted from the CD45-CD31-podoplanin+VCAM-1+ stromal cell fraction was sorted from enzymatically digested mouse LNs, cultured stromal cell lines stimulated with or without lymphotoxin (LTM-NM-2R agonistic antibody), and mouse embryonic fibroblasts (MEFs) were used for microarray analysis to assess relative gene expression.

2014-06-19 | E-GEOD-55251 | biostudies-arrayexpress

Single-cell sequencing of adipose-derived mesenchymal stromal cells and dermal fibroblasts

Project description:Single-cell sequencing of adipose-derived mesenchymal stromal cells and fibroblasts.

| EGAS00001006954 | EGA

TIMP1 overexpression mediates resistance of MCF-7 human breast cancer cells to fulvestrant and down-regulates progesterone receptor expression

Project description:High levels of Tissue Inhibitor of Metalloproteinases-1 (TIMP1) are associated with poor prognosis, reduced response to chemotherapy, and, potentially, also poor response to endocrine therapy in breast cancer patients. Our objective was to further investigate the hypothesis that TIMP1 is associated with endocrine sensitivity. We established a panel of 11 MCF-7 subclones with a wide range of TIMP1 mRNA and protein expression levels. Cells with high expression of TIMP1 versus low TIMP1 displayed significantly reduced sensitivity to the antiestrogen fulvestrant (ICI 182,780, Faslodex®), while TIMP1 levels did not influence the sensitivity to 4-hydroxytamoxifen. An inverse correlation between expression of the progesterone receptor and TIMP1 was found, but TIMP1 levels did not correlate with estrogen receptor levels or growth-promoting effects of estrogen (estradiol, E2). Additionally, the effects of fulvestrant, 4-hydroxytamoxifen, or estrogen on estrogen receptor expression were not associated with TIMP1 levels. Gene expression analyses revealed associations between expression of TIMP1 and genes involved in metabolic pathways, epidermal growth factor receptor 1/cancer signaling pathways, and cell cycle. Gene and protein expression analyses showed no general defects in estrogen receptor signaling except from lack of progesterone receptor expression and estrogen inducibility in clones with high TIMP1. The present study suggests a relation between high expression level of TIMP1 and loss of progesterone receptor expression combined with fulvestrant resistance. Our findings in vitro may have clinical implications as the data suggest that high tumor levels of TIMP1 may be a predictive biomarker for reduced response to fulvestrant.

2013-08-22 | GSE35535 | GEO

Expression Data from PtenF341V and Null Mouse Embryonic Fibroblasts

Project description:PTEN imparts tumor suppression in mice by cell autonomous and non-autonomous mechanisms. Whether these two tumor suppressor mechanisms are mediated through similar or distinct signaling pathways is not known. Here we generated and analyzed knockin mice that express a series of human cancer-derived mutant alleles of PTEN that differentially alter the Akt axis in either stromal or tumor cell compartments of mammary glands. We find that cell non-autonomous tumor suppression by Pten in stromal fibroblasts strictly requires activation of P-Akt signaling, whereas cell autonomous tumor suppression in epithelial tumor cells is independent of overt canonical pathway activation. These findings expose distinct Akt-dependent and independent tumor suppressor functions of PTEN in stromal fibroblasts and tumor cells, respectively, that can be used to guide clinical care of breast cancer patients Wild type, Pten null and PtenF341V primary mouse embryonic fibroblasts isolated from 13.5 day old embryos (E13.5) were cultured, RNA was extracted and Affymetrix gene expression arrays were performed.

2014-12-19 | E-GEOD-64302 | biostudies-arrayexpress

Homo sapiens

Project description:GPI-anchored Timp1 protein

| PRJNA173439 | ENA