Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Suppression of skin tumorigenesis in CD109-deficient mice

ABSTRACT: CD109 is a glycosylphosphatidylinositol-anchored glycoprotein that is highly expressed in several types of human cancers, particularly squamous cell carcinomas. We previously reported that CD109-deficient mice exhibit epidermal hyperplasia and chronic skin inflammation. Although we found that CD109 regulates differentiation of keratinocytes in vivo, the function of CD109 in tumorigenesis remains unknown. In this study, we investigated the role of CD109 in skin tumorigenesis using a two-stage carcinogenesis model in CD109-deficient mice with chronic skin inflammation.

ORGANISM(S): Mus musculus

PROVIDER: GSE87390 | GEO | 2016/09/28

SECONDARY ACCESSION(S): PRJNA344646

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

CD109 regulates in vivo tumor invasion in lung adenocarcinoma through TGF-β signaling

Project description:CD109 is a glycosylphosphatidylinositol-anchored glycoprotein highly expressed in several types of human malignant tumors including lung cancers. We investigated the in vivo functions of CD109 protein in malignant lung tumors. CD109+/+ and CD109-/- K-ras[LSL-G12D/+];p53[fl/fl] (KP) mice were sacrificed at 20 to 23 weeks of age and total RNA was extracted from the lung tumors. SurePrint G3 Mouse GE Microarray 8×60K Ver.2.0 were performed.

2020-10-01 | GSE155453 | GEO

Patient-derived glioblastoma stem cells transcriptome regulation by CD109

Project description:Glioma stem cells (GSCs) drive propagation and therapeutic resistance of glioblastomas, the most aggressive diffuse brain tumor. However, the molecular mechanisms that maintain the stemness and promote therapy resistance remain poorly understood. Here we study CD109 – STAT3 axis as crucial for the maintenance of stemness and tumorigenicity of GSCs and as a mediator of chemoresistance. Mechanistically, CD109 physically interacts with glycoprotein 130 (GP130) to promote activation of the IL-6/STAT3 pathway in GSCs. Genetic depletion of CD109 abolished the stemness and self-renewal of GSCs and impaired tumorigenicity. Loss of stemness was accompanied with a phenotypic shift of GSCs to more differentiated astrocytic-like cells. Importantly, genetic or pharmacologic targeting of CD109 – STAT3 axis sensitized the GSCs to chemotherapy suggesting that targeting CD109 – STAT3 axis has potential to overcome therapy resistance in glioblastoma.

2021-03-24 | GSE169418 | GEO

Cell surface processing of CD109 by meprin β leads to the release of soluble fragments and reduced expression on extracellular vesicles

Project description:Cluster of differentiation 109 (CD109) is a glycosylphosphatidylinositol (GPI) anchored protein expressed on primitive hematopoietic stem cells, activated platelets, CD4+ and CD8+ T-cells and keratinocytes. In recent years CD109 was also associated with different tumor entities and identified as a possible future diagnostic marker linked to reduced patient survival. Also, different cell signaling pathways were proposed as targets for CD109 interference including the TGFβ, JAK-STAT3, YAP/TAZ and EGFR/AKT/mTOR pathways. Here, we identify the metalloproteinase meprin β to cleave CD109 at the cell surface and thereby induce the release of cleavage fragments of different size. Major cleavage was identified within the bait region of CD109 residing in the middle of the protein. To identify the structural localization of the bait region, homology modeling and single particle analysis were applied, resulting in a molecular model of membrane associated CD109, which allows for the localization of the newly identified cleavage sites for meprin β and the previously published cleavage sites for the metalloproteinase bone morphogenetic protein 1 (BMP-1). Full-length CD109 localized on extracellular vesicles (EVs) was also identified as a release mechanism and we can show that proteolytic cleavage of CD109 at the cell surface reduces the amount of CD109 sorted to EVs. In summary, we identified meprin β as the first membrane bound protease to cleave CD109 within the bait region, provide a first structural model for CD109 and show that cell surface proteolysis correlates negatively with CD109 released on EVs.

2021-01-28 | PXD023727 | Pride

Mus musculus

Project description:Suppression of skin tumorigenesis in CD109-deficient mice

| PRJNA344646 | ENA

Expression data from RECK-overexpressing HT1080 fibrosarcoma cells

Project description:RECK, a glycosylphosphatidylinositol-anchored glycoprotein, inhibits the enzymatic activities of some matrix metalloproteinases (MMP), thereby suppressing tumor cell metastasis; however, the detailed mechanism is still obscure. In this study, we compared the gene expression profiles between mock- and RECK-transfected HT1080 cells.

2010-04-14 | GSE21306 | GEO

CD109 plays a role in osteoclastogenesis.

2013-01-29 | GSE43811 | GEO

CD109 plays a role in osteoclastogenesis.

Project description:The primary aim of this project was to identify novel factors, in particular the cell-surface protein CD109, which regulate osteoclastogenesis. Microarray analysis was performed comparing two pre-osteoclast cell lines generated from the RAW 264.7 osteoclast cell line: one that has the capacity to fuse forming large multinucleated cells and one that does not fuse. It was found that CD109 was up-regulated by > 17-fold in the osteoclast forming cell line when compared to the cell line that does not fuse. H10 (osteoclastogenic cell line) and C8 (non osteoclastogenic cell line) cells were plated for two days in 60 mm tissue culture dishes at a density of 0.5 x 10^6 in a culture medium consisting of 8 ml of Dulbecco's Modified Eagle Medium (DMEM, Life Technologies, Grand Island, NY, USA) supplemented with 10% Fetal Bovine Serum (FBS) and 10% antibiotics (164 IU/mL of penicillin G, 50 mg/ml of gentamicin, and 0.25 mg/ml of fungizone) as well as purified recombinant RANKL (60ng/ml). Following two days of culture, total RNA was extracted from the H10 and C8 cells (Qiagen RNeasy Minikit, Germantown, MD, USA) and the concentration of extracted RNA was measured (using a nanodrop method). Experiment was done in triplicates

2013-01-29 | E-GEOD-43811 | biostudies-arrayexpress

Clostridioides difficile CD109

Project description:Clostridioides difficile CD109 Genome sequencing and assembly

| PRJNA85735 | ENA

Expression data to parental A431 VS CD109 KO A431

Project description:analysis the gene expression alteration upon the loss of CD109

2019-11-19 | GSE117475 | GEO

FLOT2 promotes nasopharyngeal carcinoma progression through suppression of TGF-β pathway via facilitating CD109 expression

Project description:In nasopharyngeal carcinoma (NPC), the TGF-β/SMAD pathway genes are altered with inactive TGF-β signal, but the mechanisms remain unclear. Flotillin 2 (FLOT2) is a highly expressed protein in NPC, and is crucial for NPC progression. We show that FLOT2 negatively regulated TGF-β signaling pathway via up-regulating CD109 expression. FLOT2 increased CD109 transcription by stabilizing STAT3, which is identified as the activating transcription factor of CD109. FLOT2 interacted with STAT3 directly and increased the stability of STAT3 by inhibiting K48-linked polyubiquitination. CD109 could rescue the functional changes of NPC cells resulted from FLOT2 alteration. Expression of FLOT2 and CD109 was positively correlated, and was significantly higher in NPC tissues than in the normal nasopharyngeal epithelial tissues. Patients with high expression of both FLOT2 and CD109 presented poorer overall survival and disease-free survival compared those with high expression of one protein alone. In conclusion, FLOT2 promotes the development of NPC by inhibiting TGF-β signaling pathway via stimulating the expression of CD109 by stabilizing STAT3, which provides novel potential therapeutic strategy for NPC treatment.

2023-10-19 | GSE245418 | 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