Melanoma miRNA trafficking triggers the tumor primary niche formation
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ABSTRACT:
PROVIDER: PRJNA294464 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2016-08-09 | E-GEOD-72620 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-08-09 | GSE72620 | GEO
Project description:mRNA profiles generated from primary fibroblast upon treatment with miR-211, miR-302 or melanoma melanosomes. Abstract: Melanoma originates in the epidermis and enters the metastatic and lethal phase upon invasion into the dermis. However, the interactions between melanoma cells and the dermis prior to this invasion have been poorly studied. Here we uncover that melanoma cells directly affect the formation of the dermal tumor niche by microRNA (miRNA) trafficking prior to invading the dermis. Melanocytes, the cells of melanoma origin, are specialized in trafficking of pigment vesicles, termed melanosomes and, interestingly, melanoma cells retain this trafficking ability. In melanoma in-situ specimens, we found melanosome markers in distal fibroblasts prior to the invasion of melanoma cells into the dermis. Melanoma-derived melanosomes carry miRNAs into primary fibroblasts that trigger changes in the fibroblasts, including increased proliferation, migration, and expression of pro-inflammatory genes, all known features of cancer-associated fibroblasts (CAFs). Specifically, we found that melanosomal miRNA-211 directly targets IGF2R and leads to MAPK signaling activation in fibroblasts, which reciprocally encourages melanoma growth. Treatment of melanoma cells with a melanosome release-inhibitor prevented CAF formation. Since the first interaction of melanoma cells with blood vessels occurs in the dermis, our data suggest a promising opportunity to block melanoma cell invasion by preventing the formation of the dermal tumor niche. In the paper we showed the 10% of most differentially expressed mRNA upon miR-211, miR-320c and melanosomes treatment and overlap of 2000 downregulated mRNA upon miR-211 and melanosomes treatment with predicted target gene miR-211 and CAFs related genes Expresssion profiling was performed for primary fibroblasts transfected with miRNA-211 mimic and miRNA-320c mimic.
2016-08-09 | E-GEOD-72619 | biostudies-arrayexpress
Project description:Despite recent advancements in melanoma therapy, hepatic metastasis in malignant melanoma patients remains associated with significantly reduced overall survival rates. Given the rising prevalence of metabolic liver diseases such as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NAFLD/NASH), we investigated whether metabolic changes influence hepatic melanoma metastasis. Our study found that induction of advanced NASH in C57BL/6N mice through a choline-deficient L-amino acid (CDAA)-defined diet for ten weeks significantly increased hepatic metastasis, as demonstrated by injecting B16F10Luc2 and Wt31 melanoma cells. B16F10Luc2 cells showed heightened metastatic potential even with shorter periods of CDAA feeding before liver fibrosis developed. Conversely, hepatic steatosis induced by a high-fat diet alone did not promote increased melanoma metastasis. Early pre-fibrotic changes in the hepatic vascular niche, particularly in liver sinusoidal endothelial cells (LSECs), appeared to be responsible for the enhanced metastasis, characterized by continuous endothelial dedifferentiation and upregulation of adhesion molecules VCAM1, ICAM1, and E-selectin. Functionally, B16F10Luc2 cell retention in the hepatic vascular niche was significantly increased early after CDAA feeding, with ICAM1 inhibition leading to a notable reduction in cell retention. In summary, our findings highlight the hepatic vascular niche's sensitivity to metabolic alterations, suggesting potential avenues for preventing hepatic melanoma metastasis through angiotargeted therapies.
2025-02-05 | GSE264249 | GEO
Project description:Despite recent advancements in melanoma therapy, hepatic metastasis in malignant melanoma patients remains associated with significantly reduced overall survival rates. Given the rising prevalence of metabolic liver diseases such as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NAFLD/NASH), we investigated whether metabolic changes influence hepatic melanoma metastasis. Our study found that induction of advanced NASH in C57BL/6N mice through a choline-deficient L-amino acid (CDAA)-defined diet for ten weeks significantly increased hepatic metastasis, as demonstrated by injecting B16F10Luc2 and Wt31 melanoma cells. B16F10Luc2 cells showed heightened metastatic potential even with shorter periods of CDAA feeding before liver fibrosis developed. Conversely, hepatic steatosis induced by a high-fat diet alone did not promote increased melanoma metastasis. Early pre-fibrotic changes in the hepatic vascular niche, particularly in liver sinusoidal endothelial cells (LSECs), appeared to be responsible for the enhanced metastasis, characterized by continuous endothelial dedifferentiation and upregulation of adhesion molecules VCAM1, ICAM1, and E-selectin. Functionally, B16F10Luc2 cell retention in the hepatic vascular niche was significantly increased early after CDAA feeding, with ICAM1 inhibition leading to a notable reduction in cell retention. In summary, our findings highlight the hepatic vascular niche's sensitivity to metabolic alterations, suggesting potential avenues for preventing hepatic melanoma metastasis through angiotargeted therapies.
2025-02-05 | GSE264318 | GEO
Project description:Despite recent advancements in melanoma therapy, hepatic metastasis in malignant melanoma patients remains associated with significantly reduced overall survival rates. Given the rising prevalence of metabolic liver diseases such as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NAFLD/NASH), we investigated whether metabolic changes influence hepatic melanoma metastasis. Our study found that induction of advanced NASH in C57BL/6N mice through a choline-deficient L-amino acid (CDAA)-defined diet for ten weeks significantly increased hepatic metastasis, as demonstrated by injecting B16F10Luc2 and Wt31 melanoma cells. B16F10Luc2 cells showed heightened metastatic potential even with shorter periods of CDAA feeding before liver fibrosis developed. Conversely, hepatic steatosis induced by a high-fat diet alone did not promote increased melanoma metastasis. Early pre-fibrotic changes in the hepatic vascular niche, particularly in liver sinusoidal endothelial cells (LSECs), appeared to be responsible for the enhanced metastasis, characterized by continuous endothelial dedifferentiation and upregulation of adhesion molecules VCAM1, ICAM1, and E-selectin. Functionally, B16F10Luc2 cell retention in the hepatic vascular niche was significantly increased early after CDAA feeding, with ICAM1 inhibition leading to a notable reduction in cell retention. In summary, our findings highlight the hepatic vascular niche's sensitivity to metabolic alterations, suggesting potential avenues for preventing hepatic melanoma metastasis through angiotargeted therapies.
2025-02-05 | GSE264254 | GEO
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Project description:mRNA profiles generated from primary fibroblast upon treatment with miR-211, miR-302 or melanoma melanosomes. Abstract: Melanoma originates in the epidermis and enters the metastatic and lethal phase upon invasion into the dermis. However, the interactions between melanoma cells and the dermis prior to this invasion have been poorly studied. Here we uncover that melanoma cells directly affect the formation of the dermal tumor niche by microRNA (miRNA) trafficking prior to invading the dermis. Melanocytes, the cells of melanoma origin, are specialized in trafficking of pigment vesicles, termed melanosomes and, interestingly, melanoma cells retain this trafficking ability. In melanoma in-situ specimens, we found melanosome markers in distal fibroblasts prior to the invasion of melanoma cells into the dermis. Melanoma-derived melanosomes carry miRNAs into primary fibroblasts that trigger changes in the fibroblasts, including increased proliferation, migration, and expression of pro-inflammatory genes, all known features of cancer-associated fibroblasts (CAFs). Specifically, we found that melanosomal miRNA-211 directly targets IGF2R and leads to MAPK signaling activation in fibroblasts, which reciprocally encourages melanoma growth. Treatment of melanoma cells with a melanosome release-inhibitor prevented CAF formation. Since the first interaction of melanoma cells with blood vessels occurs in the dermis, our data suggest a promising opportunity to block melanoma cell invasion by preventing the formation of the dermal tumor niche. In the paper we showed the 10% of most differentially expressed mRNA upon miR-211, miR-320c and melanosomes treatment and overlap of 2000 downregulated mRNA upon miR-211 and melanosomes treatment with predicted target gene miR-211 and CAFs related genes
2016-08-09 | GSE72619 | GEO
Project description:Perinatal Brain Injury Triggers Niche-Specific Changes to Cellular Biogeography [MERFISH]
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