Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Down-regulation of ECRG4, a candidate tumor suppressor gene in human breast cancer

ABSTRACT: ECRG4 is a promising tumor suppressor gene (TSG) recently identified in esophageal carcinoma. Its expression and prognostic value have never been explored in breast cancer. Using DNA microarray, we examined ECRG4 mRNA expression in 353 invasive breast cancer samples. A meta-analysis was performed on a large public retrospective gene expression dataset (n=1,387) to analyze correlation between ECRG4 expression and histo-clinical features including survival.

ORGANISM(S): Homo sapiens

PROVIDER: GSE31448 | GEO | 2011/12/02

SECONDARY ACCESSION(S): PRJNA145819

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiles of Ecrg4-treated mouse microglia

Project description:Esophageal cancer-related gene 4 (Ecrg4), a hormone-like peptide, is thought to be a tumor suppressor, however little is known about the mechanism of how Ecrg4 suppresses tumorigenesis. Using the mouse glioma–initiating cell models, we identified Ecrg4 acts as a tumor suppressor in vivo. To characterize the function of Ecrg4 towards microglia, an innate immune cell in central nervous system, we performed gene expression microarray analysis for primary microglia treated with or without recombinant Fc-fused Ecrg4 fragments. We demonstrate here that Ecrg4 fragments, amino acid residues 71-132 and 133-148, which are produced by the proteolitic cleavage, induced the expression of pro-inflammatory cytokines in microglia. Thus, Ecrg4 acts as a cytokine/chemokine inducer, which activates the immune cells to eradicate tumor.

2016-09-28 | GSE87376 | GEO

Gene expression profile of Ba/F3 variant (#BEB1) cells that have binding ability to Ecrg4

Project description:Esophageal cancer-related gene 4 (Ecrg4) encodes a hormone-like peptide, and is thought to be involved in a variety of physiological phenomena including tumor suppressor function. Recent progress of Ecrg4 reveals that Ecrg4 peptides are pro-inflammatory and induce the expression of several cytokines and chemokines. However, detailed molecular mechanisms of Ecrg4 signaling, especially the receptors for Ecrg4 peptides, remain poorly understood. Here, using retrovirus-mediated expression cloning, we identified lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) as a membrane protein bound for amino acid residues 71-132 of Ecrg4, Ecrg4(71-132). Moreover, not only LOX-1 but also several scavenger receptors such as Scarf1, Cd36 and Stabilin-1 efficiently internalized Ecrg4(71-132) into cells. The broad scavenger receptor competitive inhibitor polyinosinic acid reduced both the internalization of Ecrg4(71-132) and activation of NF-kB in microglia. In addition, this activation is dependent on Myd88, an adaptor protein to recruit signaling proteins to TLR and IL-1R receptors with induction of several immune response. These data suggest that multiple scavenger receptors recognize Ecrg4(71-132) and transduce its signals along with TLR/IL-1R receptors in microglia.

2018-03-23 | GSE106400 | GEO

Proteomic Analysis on Paraffine-Archived Melanoma

Project description:The discovery of novel protein biomarkers in melanoma is crucial. Our introduction of formalin-fixed paraffin embedded (FFPE) tumor protocol provides new opportunities to understand the progression of melanoma and open the possibility to screen tens of thousands of FFPE samples deposited in tumor biobanks and available at hospital pathology departments. In our retrospective pilot study, 90 FFPE samples from 77 patients were processed. Differential quantitative protein expression was performed by high resolution mass spectrometry. The protein expression profiles were correlated with the standardized dataset of histopathologic analysis, and longitudinal therapeutical meta-data.

2022-02-17 | PXD028930 | Pride

Regulatory mechanisms of TSG-6 (TNF-alfa-induced protein-6: Tnfip6)-deficient and wild-type synovial fibroblasts

Project description:BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), and the absence of TSG-6 further increases susceptibility and local inflammatory reactions, including neutrophil invasion into the joints. To gain insight into the mechanisms of TSG-6 action, synovial fibroblasts were isolated from wild-type and TSG-6-KO mice, cultured and exposed to various agents affecting either the TSG-6 expression and/or modify the intracellular function of TSG-6. In the present microarray studies, we have identified differences in gene expression by fibroblasts isolated from wild-type or TSG-6-KO mice Keywords: Genetic modification In this study we compared the gene expression profile of 42 fibroblast cultures from mouse synovial samples. Fifteen samples were wild-type and 27 samples were TSG-6 knockout. In these two genotype groups fibroblasts were treated with TNFa, LPS, TSG-6, HA, or HA+TSG-6, and were compared to untreated samples in the same genotype group. We also compared the same treatments between KO and WT.

2011-07-04 | E-GEOD-17160 | biostudies-arrayexpress

Regulatory mechanisms of TSG-6 (TNF-alfa-induced protein-6: Tnfip6)-deficient and wild-type synovial fibroblasts

2011-07-05 | GSE17160 | GEO

NOTCH3 Blockade Inhibits Cancer Cell Plasticity through a NOTCH3/PD-L1 Oncogenic Axis in Triple Negative Breast Cancer

Project description:Triple negative breast cancer (TNBC) accounts for 15-20% of all breast cancers and mainly affects pre-menopausal and minority women. Therapeutic options are yet limited, in part because of acquisition of tumor cells with cancer stem cell (CSC) properties, leading to intrinsic resistance to chemotherapeutic agents and immune evasion capacity. Dysregulated Notch signaling has been linked to breast cancer and in this study, we demonstrate the pivotal role of NOTCH3 in inducing the enrichment of chemoresistant ALDHhigh CSCs. Significantly, selective targeting of NOTCH3 with AV-353, a novel humanized monoclonal antibody, or by shRNA-mediated knockdown, impaired the enrichment of ALDHhigh CSCs with high self-renewal capacity, induced apoptosis and enhanced chemosensitivity. AV-353 treatment similarly reduced growth of xenografted tumors in vivo. Moreover, blocking NOTCH3 by AV-353 or shRNA reduced PD-L1 expression in TNBC cells, which was linked to the inhibition of tumor growth and enhancement of CD8+ T-cell infiltration. Taken together, these findings provide preclinical evidence for NOTCH3 as a novel therapeutic target in TNBC and reveal a novel NOTCH3/PD-L1 oncogenic axis as a platform for the betterment of TNBC therapy.

2024-06-28 | GSE236140 | GEO

RNAseq of epidermis reconstructed from TSG-6-/- and TSG-6+/+ immortalized N/TERT keratinocytes and stimulated or not with interleukins 4 and 13 for 48h

Project description:TNFα-stimulated gene 6 (TSG-6) is an anti-inflammatory protein. In human epidermis, TSG-6 is secreted in extracellular matrix where it interacts with hyaluronan (HA). However, their functions are not well understood. In this study, immortalized N/TERT keratinocytes were edited by CRISPR/Cas9, used to reconstruct in vitro epidermis (RHE) and stimulated or not with interleukins 4 and 13 for 48h to mimic atopic dermatitis (AD). Two TSG-6-/- clones (respectively TSG-6-/- (a) and TSG-6-/- (b)) harboring major deletions in both alleles were selected and compared to TSG-6+/+ cells. Epidermis reconstructed from TSG-6-/- (a) and TSG-6-/- (b) exhibit normal differentiation process and morphology but show an increased HA leakage in the underlying culture medium of both TSG-6-/- RHE compared to TSG-6+/+ tissues, especially in conditions that mimic AD. While IL-4/13 treatment of RHE induces regulation of genes associated with AD, the absence of TSG-6 don’t seem to show any major transcriptomic regulation.

2021-12-30 | E-MTAB-10095 | biostudies-arrayexpress

Genome-wide expression data of breast cancer samples

Project description:DASL gene expression data of fresh-frozen breast cancer tissue samples Retrospective cohort

2014-07-09 | E-GEOD-59198 | biostudies-arrayexpress

Gene expression profiles of Ecrg4-wt, -hetero and -homo NSCs

Project description:To identify factors that increase and decrease in Ecrg4 deficient NSCs

2019-02-27 | GSE120749 | GEO

TSG-6 supports fistulizing Crohn’s disease by a mechanoregulated activation of the epithelial-to-mesenchymal transition

Project description:BACKGROUND AND AIMS: Perianal fistula represents one of the most important complications in Crohn’s Disease (CD). Epithelial-to-mesenchymal transition (EMT) has been demonstrated to play a major role in the pathogenesis, however the mechanisms driving EMT need to be clarified. Significant alterations in the tissue structural composition occur in the fistula, but how these changes promote EMT was not addressed. We aim to explore the relevance of TSG-6, a stabilizer of extracellular matrix, in the fistula pathogenesis. METHODS: Intestinal surgical specimens from perianal fistula tissue and surrounding region of fistulizing CD were analyzed histologically and by RNA sequencing (RNA-seq). Significantly modulated genes and TSG-6 expression were validated by RT-PCR, WB and immunofluorescence assays [N=20]. TSG-6 expression was reconstituted in Caco-2 cell line and primary perifistula-derived fibroblasts, and proliferative and migratory assays were performed. RESULTS: A marked different organization of extracellular matrix was found across fistula and perifistula regions with an increased expression of integrins, hyaluronan synthases, TSG-6 and MMPs in the fistula. TSG-6 overexpression in Caco-2 cells reduced proliferation, promoted the EMT transcription factor SNAIL, and, in co-stimulation with TGFβ1, migration. The acquisition of TSG-6 increased SNAI1 and hyaluronan synthases levels, and led to activated phenotype of perifistula-derived fibroblasts. Positive Pearson correlation was observed between TSG-6 expression and mechanosensitive proteins in fistula tissue. CONCLUSIONS: By mediating changes in the extracellular matrix organization, TSG-6 triggers the EMT transcription factor SNAIL through the activation of mechanosensitive proteins. These data point to TSG-6 as a new potential target for the treatment of perianal fistula.

2023-01-04 | GSE157020 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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