Similar Datasets
Project description:Expression data to parental A431 VS CD109 KO A431
| PRJNA482298 | ENA
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: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
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: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: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.
2013-01-29 | GSE43811 | GEO
Project description:Clostridioides difficile CD109 Genome sequencing and assembly
| PRJNA85735 | ENA
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 encodes a GPI-linked glycoprotein that acts as a signaling modulator in the TGF-β pathway. CD109 has emerged in several genome-wide association studies as linked to coronary artery disease, myocardial infarction, and angina pectoris. Heterozygous loss-of-function mutations in CD109 have also been reported in patients with congenital heart defects, suggesting potential developmental relevance, though CD109 has never been investigated in the context of cardiovascular development. We previously identified Cd109 upregulation in murine atrioventricular valves undergoing myxomatous degeneration following a reduction of epicardial-derived cells. Here, we characterize Cd109 expression in the murine cardiovascular system and assess its function during development using in vitro and in vivo approaches. We found that Cd109 is strongly expressed in the endothelium of the coronary vasculature and in an endocardial-derived subpopulation in the atrioventricular valves. This expression persists through key stages in cardiovascular development. Western blotting and immunostaining confirm endothelial expression in heart and lung tissues. siRNA knockdown of CD109 in primary human endothelial cells led to dysregulation of vascular development pathways and decreased tube formation capacity. We generated Tie2Cre;Cd109fl/fl mice, eliminating Cd109 expression from heart and lung tissues without overt morphological consequences. Together, these results establish Cd109 as a useful marker of coronary vasculature in the heart and indicate that endothelial lineage-specific deletion of Cd109 does not cause gross morphological defects during cardiac development. The transcriptional and functional changes observed in endothelial cells in vitro suggest that additional studies will be necessary to define contexts in which Cd109 influences vascular biology.
2026-05-03 | GSE329398 | GEO
Project description:Although immune checkpoint inhibitors (ICIs) have improved the prognosis of melanoma, overcoming acquired resistance remains a challenge. The most critical mechanism is B2M mutation-mediated major histocompatibility complex (MHC) class I loss. Conversely, resistance mechanisms other than B2M mutations might be surmountable, although most of them are not yet fully understood. This study aimed to explore the novel mechanisms of acquired resistance in the absence of MHC class I loss. Previously, we established a pair of melanoma cell lines and cultured tumor-infiltrating lymphocytes (TILs) derived from an ICI-resistant melanoma patient with B2M mutation. Autologous TILs were unable to recognize the melanoma cells (MEL01), although genetic transduction of wild-type B2M (MEL01-B2M) reversed this phenomenon. To identify resistance mechanisms other than B2M mutation, we generated TIL-resistant MEL01-B2M cells by in vitro long-term co-culture (MEL01-B2M-R) and compared gene expression profiles between MEL01-B2M and MEL01-B2M-R. CD109 expression in MEL01-B2M-R cells was reduced by < 20%. Although CD109 has attracted attention as a negative regulator of transforming growth factor beta in allergic diseases, its effect on TILs, which play a central role in the efficacy of ICIs, remains unknown. Immunohistochemical analysis of 142 patients with melanoma revealed that low CD109 expression was associated with poor prognosis, regardless of MHC class I retention in melanoma tissues. In the co-culture assay, the knockout of CD109 in melanoma cells significantly impaired recognition and killing by specific TILs. These findings suggest that CD109 may serve as a predictive biomarker of ICI efficacy and as a novel therapeutic target for overcoming ICI resistance.
2025-09-30 | GSE309150 | GEO