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

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

PROVIDER: PRJNA1028312 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26389229_1.fastq.gz	Fastqsanger.gz
	SRR26389229_2.fastq.gz	Fastqsanger.gz
	SRR26389230_1.fastq.gz	Fastqsanger.gz
	SRR26389230_2.fastq.gz	Fastqsanger.gz
	SRR26389231_1.fastq.gz	Fastqsanger.gz

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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

Suppression of skin tumorigenesis in CD109-deficient mice

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.

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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.

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Expression data for human nasopharyngeal carcinoma cell line HK1 stimulated with EGF or TGF-Î² recombinant protein.

Project description:As regulators in gene expression, microRNAs take part in most biological process including cell differentiation, apoptosis, cell cycle and epithelial-to-mesenchymal transition (EMT). In order to evaluate their roles during the growth factors-induced EMT process, microRNA expression profile changes induced by EGF or TGF-Î² treatment on nasopharyngeal carcinoma cell line HK-1 cells were analyzed by means of the Affymetrix genome wide microarray system. Human nasopharyngeal carcinoma cell line HK-1 was starved for 12 hours before stimulation with EGF (50 ng/mL) or TGF-Î² (10ng/ml) or Control (PBS) for 36 hours in RPMI-1640 medium (with 1% serum) to establish the in vitro model of EMT. Total RNA were extracted and detected by AffymetrixÂ® GeneChipÂ® miRNA Arrays.

2015-12-17 | E-GEOD-64281 | biostudies-arrayexpress

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

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

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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

CD109 plays a role in osteoclastogenesis.

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Clostridioides difficile CD109

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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

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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