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Podoplanin is a marker but no driver for malignant progression in glioblastoma

ABSTRACT: Podoplanin is a marker but no driver for malignant progression in glioblastoma

PROVIDER: PRJNA473086 | ENA |

REPOSITORIES: ENA

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Podoplanin is a marker but no driver for malignant progression in glioblastoma

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Gene expression profiling of MCF7 breast cancer xenografts overexpressing podoplanin (human array)

Project description:Expression of the membrane glycoprotein podoplanin is upregulated in several human cancers and might be associated with their malignant progression. The exact biological function and molecular targets of cancer cell-expressed podoplanin have remained unclear, however. Here, we ectopically overexpressed podoplanin in a human breast carcinoma xenograft model to study its role in cancer progression. To identify molecular mediators of podoplanin-induced effects we compared transcriptional profiles of podoplanin-overexpressing and control tumors. Keywords: comparative transcriptional profiling

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Gene expression profiling of tumor stroma of MCF7 breast cancer xenografts overexpressing podoplanin (mouse array)

Project description:Expression of the membrane glycoprotein podoplanin is upregulated in several human cancers and might be associated with their malignant progression. The exact biological function and molecular targets of cancer cell-expressed podoplanin have remained unclear, however. Here, we ectopically overexpressed podoplanin in a human breast carcinoma xenograft model to study its role in cancer progression. To identify potential molecular mediators of podoplanin-induced effects in the murine tumor stroma we compared transcriptional profiles of podoplanin-overexpressing and control tumors using mouse microarrays. Keywords: comparative transcriptional profiling

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Transcription profiling of lymphatic endothelial cell subtypes expressing high and low levels of podoplanin

Project description:We microprepared native mammary skin resections from healthy female donors (breast size reduction) by a combination of enzymatic and mechanical treatment. The resulting suspensions of single dermal cells were then subjected to FACSorting using antibodies against the lymphovascular marker protein podoplanin and the panendothelial protein CD31 as positive and the leukocytic protein CD45 as negative markers. We aimed at separating lymphatic vascular endothelial cells (LECs) from blood vascular endothelial cells (BECs) in order to characterize their moelcular and functional phenotypes in health and disease. We found that lymphatic endothelial cells consisted of two instead of only one cell population. Their discrimination marker was high versus low expression of podoplanin surface protein, respectively. Especially, the low-podoplanin expressors were undescribed. Thus, we screened for their transcription profile using U133A. We identified specific marker genes and finally have assigned a specific function to the novel LEC subpopulation unknown up to now. Importantly, we did not use lysates from cell culture, but from ex vivo cells. Thus, there was no treatment of cells except processing the samples on ice.

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Driver gene alterations and activated signaling pathways toward malignant progression of gastrointestinal stromal tumors

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Effect of podoplanin depletion on gene expressions in canine melanoma cell lines

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RNA-seq analysis of control and podoplanin knockdown lymphatic endothelial cells

Project description:To determine the transcriptome changes after podoplanin was knocked down in human lymphatic endothelial cells Human lymphatic endothelial cells were transfected with control siRNA and podoplanin siRNA (N=2 for each group). After 48 hours, total RNA was isolated and processed for RNA-seq.

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RNA-seq analysis of control and podoplanin knockdown lymphatic endothelial cells

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PD-1 marks dysfunctional regulatory T cells in malignant glioblastoma

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