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Retinoic acid inhibits tumor-associated mesenchymal stromal cell transformation in melanoma

ABSTRACT: Retinoic acid inhibits tumor-associated mesenchymal stromal cell transformation in melanoma

PROVIDER: PRJNA715445 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13997134_1.fastq.gz	Fastqsanger.gz
	SRR13997134_2.fastq.gz	Fastqsanger.gz
	SRR13997135_1.fastq.gz	Fastqsanger.gz
	SRR13997135_2.fastq.gz	Fastqsanger.gz
	SRR13997136_1.fastq.gz	Fastqsanger.gz

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Retinoic acid inhibits tumor-associated mesenchymal stromal cell transformation in melanoma

Project description:Bone marrow mesenchymal stem/stromal cells (BMSCs) can be transformed into tumor-associated MSCs (TA-MSCs) within the tumor microenvironment to facilitate tumor progression. However, the underline mechanism and potential therapeutic strategy remain unclear. Here, we explored that interleukin 17 (IL-17) cooperating with IFNγ transforms BMSCs into TA-MSCs, which promotes tumor progression by recruiting macrophages/monocytes and myeloid-derived suppressor cells (MDSCs) in murine melanoma. IL-17 and IFNγ transformed TA-MSCs have high expression levels of myelocyte-recruiting chemokines (CCL2, CCL5, CCL7, and CCL20) mediated by activated NF-κB signaling pathway. Furthermore, retinoic acid inhibits NF-κB signaling, decreases chemokine expression, and suppresses the tumor-promoting function of transformed TA-MSCs by prohibiting the recruitment of macrophages/monocytes and MDSCs in the tumor microenvironment. Overall, our findings demonstrate that IL-17 collaborating with IFNγ to induce TA-MSC transformation, which can be targeted by RA for melanoma treatment.

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Retinoic Acid Inhibits Tumor-Associated Mesenchymal Stromal Cell Transformation in Melanoma.

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Proteomics Analysis of Human Mesenchymal Stromal/Stem Cell Sarcomagenesis Model Identifies ALDH1A3 and CD99 as Potential Targets in the Transformation Process

Project description:Mesenchymal stromal/stem cells (MSC) may represent the cell-of-origin for sarcoma development. A collection of human MSCs sequentially mutated with an increasing number of oncogenic hits served to recreate a step-wise process of sarcomagenesis. To identify potential protein targets of interest in the MSC-sarcoma transformation process, quantitative mass spectrometry based (LC-MS/MS) proteomics was performed. Among the proteins hits identified as significantly regulated in the transformation process ALDH1A3 and CD99 were selected and further studied. Both ALDH1A3 abundance levels and activity were significantly up-regulated in early phase (immortalized) and fully transformed (sarcoma forming) cells as compared to normal MSCs. Inversely, CD99 total protein and cell-surface abundance levels were down-regulated in immortalized and transformed MSCs. Down-regulated CD99 was also identified in several human bone and soft tissue sarcoma subtypes. Proteomics investigation of a MSC-transformation model of sarcoma has yielded ALDH1A3 and CD99 as potential targets for sarcomagenesis that may contribute to a greater understanding of the disease and the development of novel therapeutic approaches.

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Stromal vascular fraction inhibits inhibits kidney fibrosis and inflammation in UUO mice

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Aged and BRCA mutated stromal cells drive epithelial cell transformation

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MicroRNA-127-3p inhibits the in vitro osteogenic differentiation of bone marrow-derived mesenchymal stromal cells

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The transcriptional repressor SNAI2 impairs neuroblastoma differentiation and inhibits response to retinoic acid therapy

Project description:The transcriptional repressor SNAI2 impairs neuroblastoma differentiation and inhibits response to retinoic acid therapy

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