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Expression data from second oncogene expressing Melanoma Cells.

ABSTRACT: Expression data from second oncogene expressing Melanoma Cells.

PROVIDER: PRJNA506456 | ENA |

REPOSITORIES: ENA

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Expression data from second oncogene expressing Melanoma Cells.

Project description:Among the myriad tumors analyzed to date, cutaneous malignant melanomas bear some of the highest mutational burdens. Thus, it is somewhat surprising that oncogene exclusion between is so pronounced in melanomas where there is only a single melanoma out of 366 sequenced specimens which harbors concurrent BRAF(V600E/M) and NRAS(G13R) mutations (TCGA-ES-A2NC Sample; WWW.bioportal.org), In this senario some NRAS and BRAF mutations co-expressing cells show slow growth phenotypes by under study mechanism. We used Affymetrix GeneChip Expression Arrays to detail the global programme of gene expression underlying oncogenic exclusion and identified distinct classes of up and down-regulated genes during this process.

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Project description:Gene expression SK-Mel-103 melanoma cell line to find genes controled by DEK oncogene

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Second-Hand Melanoma Melanosomes Regulate Diversity Among Tumor-Associated Macrophages

Project description:Extracellular vesicles (EVs) are a key form of cell-to-cell communication. Here we reveal a new mode of communication involving the large EVs, melanosomes. Unlike small EVsexosomes, which are dissolved in the receiver cell, melanosomes stay intact within them, gain a unique protein signature, and can then be further transferred to another cell, a state we term “second-hand EVs”. We found that melanoma-secreted melanosomes uptaken by and then released from epidermal keratinocytes or dermal fibroblasts can be further engulfed by resident macrophages. The respective consequence for macrophages is polarization into pro-tumor or pro-immune-cell-infiltration phenotypes. Fibroblasts load melanosomes with AKT1, which induces VEGF secretion from macrophages in an mTOR-dependent manner, promoting angiogenesis and metastasis in-vivo. In melanoma patients, macrophages co-localized with AKT1, were correlated with disease aggressiveness, and immunotherapy non-responders were enriched in macrophages containing melanosome markers. Thus, the network of interactions via second-hand EVs helps form the metastatic niche. Since macrophage heterogeneity is pivotal in advancement of cancer, our data suggest an opportunity to halt melanoma progression by blocking the melanosome cues of macrophage diversification.

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Second-Hand Melanoma Melanosomes Regulate Diversity Among Tumor-Associated Macrophages

Project description:Second-Hand Melanoma Melanosomes Regulate Diversity Among Tumor-Associated Macrophages

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Second-Hand Melanoma Melanosomes Regulate Diversity Among Tumor-Associated Macrophages

Project description:Extracellular vesicles (EVs) are a key form of cell-to-cell communication. Here we reveal a new mode of communication involving the large EVs, melanosomes. Unlike small EVs, which are dissolved in the receiver cell, melanosomes stay intact within them, gain a unique protein signature, and can then be further transferred to another cell, a state we term “second-hand EVs”. We found that melanoma-secreted melanosomes uptaken by and then released from epidermal keratinocytes or dermal fibroblasts can be further engulfed by resident macrophages. The respective consequence for macrophages is polarization into pro-tumor or pro-immune-cell-infiltration phenotypes. Fibroblasts load melanosomes with AKT1, which induces VEGF secretion from macrophages in an mTOR-dependent manner, promoting angiogenesis and metastasis in-vivo. In melanoma patients, macrophages co-localized with AKT1, were correlated with disease aggressiveness, and immunotherapy non-responders were enriched in macrophages containing melanosome markers. Thus, the network of interactions via second-hand EVs helps form the metastatic niche. Since macrophage heterogeneity is pivotal in advancement of cancer, our data suggest an opportunity to halt melanoma progression by blocking the melanosome cues of macrophage diversification.

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Transcriptome analysis of melanoma cells stably expressing BMP6

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Transcriptome analysis of melanoma cells stably expressing BMP6

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Project description:Gene expression analysis of miR-214 over-expressing melanoma cells (MA-2)

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