Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification and Validation of Genes with Expression Patterns Inverse to Multiple Metastasis Suppressor Genes in Breast Cancer Cell Lines

ABSTRACT: Metastasis suppressor genes (MSGs) have contributed to an understanding of regulatory pathways unique to the lethal metastatic process. When re-expressed in experimental models, MSGs block cancer spread to, and colonization of distant sites without affecting primary tumor formation. On a single MSG basis, genes have been identified with expression patterns inverse to a MSG, and found to encode functional, druggable signaling pathways. We now hypothesize that common signaling pathways mediate the effects of many MSGs. By gene expression profiling of human MCF7 breast carcinoma cells expressing a scrambled siRNA or siRNAs to each of 19 validated MSGs (NME1, BRMS1, CD82, CDH1, CDH2, CDH11, CASP8, MAP2K4, MAP2K6, MAP2K7, MAPK14, GSN, ARHGDIB, AKAP12, DRG1, CD44, PEBP1, RRM1, KISS1), we identified genes whose expression was significantly opposite to at least five MSGs. We used microarrays to evaluate the modification in gene expression profile after donregulation of multiple metastasis suppressors (NME1, BRMS1, CD82, CDH1, CDH2, CDH11, CASP8, MAP2K4, MAP2K6, MAP2K7, MAPK14, GSN, ARHGDIB, AKAP12, DRG1, CD44, PEBP1, RRM1, KISS1) in the breast cancer cell line, MCF7.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53668 | GEO | 2013/12/27

SECONDARY ACCESSION(S): PRJNA232604

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Identification and Validation of Genes with Expression Patterns Inverse to Multiple Metastasis Suppressor Genes in Breast Cancer Cell Lines

Project description:Metastasis suppressor genes (MSGs) have contributed to an understanding of regulatory pathways unique to the lethal metastatic process. When re-expressed in experimental models, MSGs block cancer spread to, and colonization of distant sites without affecting primary tumor formation. On a single MSG basis, genes have been identified with expression patterns inverse to a MSG, and found to encode functional, druggable signaling pathways. We now hypothesize that common signaling pathways mediate the effects of many MSGs. By gene expression profiling of human MCF7 breast carcinoma cells expressing a scrambled siRNA or siRNAs to each of 19 validated MSGs (NME1, BRMS1, CD82, CDH1, CDH2, CDH11, CASP8, MAP2K4, MAP2K6, MAP2K7, MAPK14, GSN, ARHGDIB, AKAP12, DRG1, CD44, PEBP1, RRM1, KISS1), we identified genes whose expression was significantly opposite to at least five MSGs. We used microarrays to evaluate the modification in gene expression profile after donregulation of multiple metastasis suppressors (NME1, BRMS1, CD82, CDH1, CDH2, CDH11, CASP8, MAP2K4, MAP2K6, MAP2K7, MAPK14, GSN, ARHGDIB, AKAP12, DRG1, CD44, PEBP1, RRM1, KISS1) in the breast cancer cell line, MCF7. MCF7 cell line was transfected with siRNA targeting each of 19 metastasis suppressors (NME1, BRMS1, CD82, CDH1, CDH2, CDH11, CASP8, MAP2K4, MAP2K6, MAP2K7, MAPK14, GSN, ARHGDIB, AKAP12, DRG1, CD44, PEBP1, RRM1, KISS1). Two siRNA sequences (siRNA1 and siRNA2) were used for each metastasis suppressor. Two time points (48hr and 96hr) were considered as end of transfection in order to measure early and late effects of the metastasis suppressors downregulation.

2013-12-27 | E-GEOD-53668 | biostudies-arrayexpress

Loss of BRMS1 promotes a mesenchymal phenotype through regulation of Twist1

Project description:Analysis of BRMS1 KD-induced EMT in non-samll cell lung cancer at gene expression level. The hypothesis tested in the present study was that BRMS1 KD induces EMT through differential regulation of EMT genes and Twist1 KD restores the epithelial phenotype in cells with BRMS1 KD. Results provide important information of biological functions in lung cancer which BRMS1 KD involves in, such as EMT, signaling, biological adhesion, immune system process, response to stimulus, and so on.

2014-11-12 | GSE62359 | GEO

Identification of a gene expression signature associated with the metastasis suppressor function of NME1

Project description:Transciptome analysis using a panel of WM793 melanoma cell lines following stable overexpression of wild-type or mutant forms of human NME1 NME1 is well known for its ability to suppress melanoma metastasis, however the means by which NME1 accomplishes this remains controversial. Herein, we utilized a bioinformatics approach to systematically identify effector genes of NME1’s metastasis suppressor function by tracking genes regulated by wild-type NME1 but not by metastasis suppressor deficient mutants of NME1. This approach identified a number of novel genes, such as ALDOC, CXCL11, LRP1b and XAGE1 as well as known targets of NME1 such as NETO2. Our NME1-mediated Metastasis Suppressor Signature (MSS) was capable of identifying subpopulations of metastatic melanoma patients with prolonged progression free survival. Interestingly, when patients were clustered by an extension of the MSS, two populations of metastatic melanoma patients were identified with significantly lowered overall and progression free survival times. Together, these data demonstrate that NMEl is a powerful tool for identifying genes that both promote and inhibit melanoma metastasis.

2017-08-22 | GSE85978 | GEO

The molecular phenotype of kisspeptin neurons in the medial amygdala of female mice

Project description:Little is known about how Kiss1 cells in the medial amygdala (MeA) are regulated and what other gene transcripts are produced by MeA Kiss1 neurons. Estradiol upregulates Kiss1 expression in the medial amygdala (MeA), but it remains unknown if estradiol regulates other gene transcripts in MeA Kiss1 cells. The goal of this study is to identify novel gene transcripts produced by MeA Kiss1 cells and to determine how estradiol regulates the expression of these transcripts. We selectively isolated mRNA from Kiss1 cells in the MeA of female mice using Ribotag transgenic mice, immunoprecipitation, and RNA-seq. Over 13,000 gene transcripts produced by MeA Kiss1 cells were identified, but only 45 of these transcripts had expression levels altered by estradiol.

2023-02-13 | GSE224788 | GEO

Gene expression in AVPV kisspeptin cells

Project description:Estrogen stimulates Kiss1 gene expression in AVPV cells in the brain, but whether estrogen regulates other genes in AVPV Kiss1 cells has not been determined. To provide a more detailed profiling of co-expressed genes in AVPV Kiss1 cells and determine how estrogen alters gene expression levels, we selectively isolated mRNAs from murine AVPV Kiss1 cells using transgenic-mediated immunoprecipitation and performed RNA-seq. This identified >13,000 mRNAs co-expressed in AVPV Kiss1 cells, including multiple transcripts that were positively or negatively regulated by estrogen.

2021-05-26 | GSE168134 | GEO

Extracellular Vesicle-Mediated Metastasis Suppressors NME1 and NME2 Modify Lipid Metabolism in Fibroblasts

Project description:Our aim was to understand how vesicular NME1 and NME2 released by breast cancer cells influence the tumour microenvironment. As a model, we used human invasive breast carcinoma cells overexpressing NME1 or NME2, and first analysed in detail the presence of both isoforms in EV subtypes by capillaryWestern immunoassay (WES) and immunoelectron microscopy. Data obtained by both methods showed that NME1 was present in medium-sized EVs or microvesicles, whereas NME2 was abundant in both microvesicles and small-sized EVs or exosomes. Next, human skin-derived fibroblasts were treated with NME1 or NME2 containing EVs, and subsequently mRNA expression changes in fibroblasts were examined. RNAseq results showed that the expression of fatty acid and cholesterol metabolism-related genes was decreased significantly in response to NME1 or NME2 containing EV treatment. We found that FASN (fatty acid synthase) and ACSS2 (acyl-coenzyme A synthetase short-chain family member 2), related to fatty acid synthesis and oxidation, were underexpressed in NME1/2-EV-treated fibroblasts. Our data show an emerging link between NME-containing EVs and regulation of tumour metabolism.

2022-08-21 | GSE211556 | GEO

Expression data from murine adipose tissue

Project description:Our previous studies have linked Trans-fat and monosodium glutamate (MSG) to the development of Nonalcoholic Fatty Liver Disease (NAFLD). We have also shown that MSG can interact with another commonly consumed food additive, aspartame, to impair glucose homeostasis, which is also disrupted in NAFLD. This most recent nutrigenomic study shows how aspartame, MSG and Trans-fat can unfavorably alter hepatic and adipose tissue gene expression. We used microarray analysis to examine changes in adipose gene transcription in response to TFA MSG and/or ASP feeding in male C57Bl/6J mice.

2015-06-03 | GSE38445 | GEO

Expression data from murine liver tissue

Project description:Our previous studies have linked Trans-fat and monosodium glutamate (MSG) to the development of Nonalcoholic Fatty Liver Disease (NAFLD). We have also shown that MSG can interact with another commonly consumed food additive, aspartame, to impair glucose homeostasis, which is also disrupted in NAFLD. This most recent nutrigenomic study shows how aspartame, MSG and Trans-fat can unfavorably alter hepatic and adipose tissue gene expression. We used microarray analysis to examine changes in liver gene transcription in response to TFA MSG and/or ASP feeding in male C57Bl/6J mice.

2015-06-03 | GSE38444 | GEO

The Major Surface Glycoprotein of Pneumocystis murina Does not Activate Dendritic Cells

Project description:The major surface glycoprotein (Msg) is the most abundant surface protein of Pneumocystis species. Given that Msg is present on both the cyst and trophic form of Pneumocystis, and dendritic cells play a critical role in initiating host immune responses, we undertook studies to examine activation of bone marrow-derived myeloid dendritic cells by Msg purified from P. murina. Incubation of dendritic cells with Msg did not lead to increased expression of CD40, CD80, CD86, or MHCII, or increased secretion of any of 10 cytokines. Microarray analysis identified very few differentially expressed genes. In contrast, LPS activated dendritic cells by all of these assays. However, Msg did bind to mouse mannose macrophage receptor and human DC-SIGN, two C-type lectins expressed by dendritic cells that are important in recognition of pathogen-associated high mannose glycoproteins. Deglycosylation of Msg demonstrated that this binding was dependent on glycosylation. These studies suggest that Pneumocystis has developed a mechanism to avoid activation of dendritic cells, potentially by the previously identified loss of genes that are responsible for the high level of protein mannosylation found in other fungi.

2018-12-26 | GSE112229 | GEO

Methylation of HBP1 by PRMT1 inhibits its tumor-suppressive function through regulating 2 GSN-mediated actin cytoskeleton remodeling

Project description:HBP1 is a sequence-specific transcription factor which acts as a tumor inhibitor. HBP1 exerts tumor-suppressive function through regulating the expression of many genes during cell metabolism and cell cycle process. Posttranslational modification of HBP1 is crucial for its function. In this study, we found that HBP1 was methylated at R378 by PRMT1, which decreased 16 HBP1 protein stability by promoting its ubiquitination and proteasome-mediated degradation. PRMT1-mediated methylation of HBP1 could alleviate the repressive effects of HBP1 on tumor metastasis and growth through regulation of GSN expression. GSN was identified as a novel target gene of HBP1. Methylation of HBP1 promoted actin cytoskeleton remodeling and tumor progression by downregulating GSN levels. The methylated HBP1-GSN axis was also associated with the clinical outcomes of cancer patients. Targeting methylated HBP1-GSN axis may provide a therapeutic strategy for cancer. Significance: This investigation elucidated the mechanism of how methylation of HBP1 at R378 inhibits its tumor-suppressive function and promotes actin cytoskeleton remodeling, thus providing the strategy for targeting HBP1 during cancer treatment.

2022-06-19 | GSE205932 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data