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

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

PROVIDER: PRJNA1032944 | ENA |

REPOSITORIES: ENA

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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.

2023-12-31 | PXD046421 | Pride

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.

2023-12-31 | GSE246446 | GEO

Expression data from second oncogene expressing Melanoma Cells.

Project description:Expression data from second oncogene expressing Melanoma Cells.

| PRJNA506456 | ENA

Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

2012-03-27 | GSE36810 | GEO

Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

Project description:Second-hand smoke (SHS) exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero exposure and adult exposure to SHS in adult mouse lungs. Left lungs from Balb/c male mice were collected at 15 weeks of age for RNA extraction and hybridization on Affymetrix mouse 430 2.0 microarrays. Based on their smoke exposure status, there are 4 groups of mice, each exposed in-utero to filtered-air or SHS and as an adult to filtered-air or SHS. We extracted RNA from 4 animals from each group for microarray analysis (N = 16 samples).

2012-03-26 | E-GEOD-36810 | biostudies-arrayexpress

Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BLNCR1 to regulate melanoma cell migration

Project description:This SuperSeries is composed of the following subset Series: GSE33092: Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BLNCR1 to regulate melanoma cell migration [HT-seq] GSE37132: Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BLNCR1 to regulate melanoma cell migration [Affymetrix] Refer to individual Series

2012-04-27 | E-GEOD-37169 | biostudies-arrayexpress

Heart fields auto-regulate second heart field cell fate via Wnt secretion

Project description:Heart fields auto-regulate second heart field cell fate via Wnt secretion

| PRJNA694043 | ENA

Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma

Project description:Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma

| PRJNA420852 | ENA

MicroRNA of exosome in Hand, foot and mouth disease serum samples

Project description:The some biomarkers can be found by pairwise comparison. They can distinguish between extremely severe Hand,foot and mouth disease and mild Hand,foot and mouth disease,moreover,they can applied to diagnose extremely severe Hand,foot and mouth disease mild Hand,foot and mouth disease vs.control; extremely severe Hand,foot and mouth disease vs.control; extremely severe Hand,foot and mouth disease vs.mild Hand,foot and mouth disease,verification by qRT-PCR

2013-11-27 | E-GEOD-52780 | biostudies-arrayexpress

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.

2018-11-22 | GSE122835 | GEO

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