CD109 plays a role in osteoclastogenesis.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE43811 | GEO | 2013/01/29
SECONDARY ACCESSION(S): PRJNA187486
REPOSITORIES: GEO
Similar Datasets
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
Project description: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.
2016-09-28 | GSE87390 | GEO
Project description:In order to determine the role of Cd109 in regulating metastatic ability and identify Cd109-dependent transcriptonal targets in metastatic lung adenocarcinoma, we sequenced the mRNA from 3 mouse metastasis cell lines. Each of these cell lines (889PF-shGFP, 889PF-shCd109#1, and 889PF-shCd109#2) were derived from the same parental cell line 889PF. 889PF was derived from the pleural fluid of a Kras LSL G12D, p53 flox/flox 129S1/SvlmJ mouse model of metastatic lung adenocarcinoma. A comparison of shGFP and shCd109 cell lines reveals Cd109-dependent changes in the metastatic transcriptome.
2017-02-06 | GSE84448 | GEO
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
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
Project description:Osteoclasts are multinucleated cells specialized in degrading the mineralized bone matrix. Osteoclast differentiation and function are tightly regulated, to prevent excessive or insufficient bone resorption. Several control mechanisms participate in modulating osteoclastogenesis, and an increasing number of reports describe the role of microRNAs (miRNAs) in this process. Disrupting the expression of specific miRNAs can result in alterations of osteoclast formation and bone homeostasis. We and others have previously characterized 9 miRNAs whose levels change during osteoclast differentiation, and identified some of the target genes that mediate their function. However, little is known about changes in the miRNA expression profile during osteoclastogenesis. In this study, we isolated a murine primary bone marrow population enriched for osteoclast precursors, and used the Agilent microarray platform to analyze the expression of mature miRNAs after 1, 3, and 5 days of RANKL-driven differentiation. 93 miRNAs showed greater than 2 fold-change during these early, middle, and late stages of osteoclastogenesis. Many of these miRNAs were detected for the first time in osteoclasts, and we validated the expression of selected miRNAs by quantitative RT-PCR. We identified clusters of differentially expressed miRNAs, and performed computational analyses to predict functional pathways that may be regulated by these miRNAs. Several miRNAs were predicted to regulate genes involved in cytoskeletal remodeling, a crucial mechanism for the migration of osteoclast precursors, their maturation, and bone resorbing activity. Our results suggest that clusters of miRNAs differentially expressed during the course of osteoclastogenesis converge on the regulation of several key functional pathways. Overall, this study identified miRNAs expressed during early, middle and late osteoclastogenesis, contributing to understanding the molecular mechanisms regulating this complex differentiation process. Mouse primary bone marrow cultures were enriched for osteoclast precursors by depletion of B220/CD45R+ and CD3+ cells (B and T lymphocytes, respectively). Cells were differentiated with M-CSF and RANKL, and miRNA expression was analyzed at days 1, 3, and 5. Four biological replicates for each time point were used.
2015-12-31 | E-GEOD-53017 | biostudies-arrayexpress
Project description:Clostridioides difficile CD109 Genome sequencing and assembly
| PRJNA85735 | ENA
Project description:analysis the gene expression alteration upon the loss of CD109
2019-11-19 | GSE117475 | GEO
Project description:Osteoclasts are large multinucleated cells that arise from the fusion of cells from the monocyte/macrophage lineage. Osteoclastogenesis is mediated by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-kB ligand (RANKL) and involves a complex multistep process that requires numerous other elements, many of which remain undefined. The primary aim of this project was to identify novel factors which regulate osteoclastogenesis. To carry out this investigation, microarray analysis was performed comparing two pre-osteoclast cell lines generated from RAW264.7 macrophages: 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, at day 2 of the differentiation process. Results obtained with microarray were confirmed by RT-qPCR and Western blot analyses in the two cell lines, in the parental RAW264.7 cell line, as well as primary murine monocytes from bone marrow. A significant increase of CD109 mRNA and protein expression during osteoclastogenesis occurred in all tested cell types. In order to characterize the role of CD109 in osteoclastogenesis, CD109 stable knockdown cell lines were established and fusion of osteoclast precursors into osteoclasts was assessed. It was found that CD109 knockdown cell lines were less capable of forming large multinucleated osteoclasts. It has been shown here that CD109 is expressed in monocytes undergoing RANKL-induced osteoclastogenesis. Moreover, when CD109 expression is suppressed in vitro, osteoclast formation decreases. This suggests that CD109 might be an important regulator of osteoclastogenesis. Further research is needed in order to characterize the role played by CD109 in regulation of osteoclast differentiation.
| S-EPMC3625217 | biostudies-literature
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