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Expression data to parental A431 VS CD109 KO A431

ABSTRACT: Expression data to parental A431 VS CD109 KO A431

PROVIDER: PRJNA482298 | ENA |

REPOSITORIES: ENA

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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

human epidermoid carcinoma cell: Control (A431-P cells) vs. highly invasive subline (A431-III cells)

Project description:Transcriptional profiling of human epidermoid carcinoma cell comparing control A431-P cells with highly invasive subline A431-III cells No treatmentt, A431-P cells vs. A431-III cells. A431-P cells are used as a reference to invstigate A431-III cells.

2013-06-18 | E-GEOD-47996 | biostudies-arrayexpress

human epidermoid carcinoma cell: Control (A431-P cells) vs. highly invasive subline (A431-III cells)

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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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Global transcriptome profiling of the 889PF mouse pleural fluid disseminating tumour cell-derived cell line, with or without Cd109 knockdown

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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.

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WT vs. NKR-P1B KO

Project description:WT vs. NKR-P1B KO

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Comparing the difference in gene expression between TDAG51 WT vs TDAG51 KO, and TDAG51 KO Tg vs TDAG51 KO

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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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