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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.

2021-03-19 | GSE169145 | GEO

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

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Mesenchymal stromal cell (MSC) Metabolite MS study

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Human intestinal stromal cells promote homeostasis in normal mucosa but inflammation in Crohn's disease in a retinoic acid-deficient manner

Project description:Stromal cell (SC) contributions to intestinal inflammation are inadequately understood. Here we show that CD90+vimentin+SMA- SCs isolated from Crohn’s disease intestine (Crohn’s SCs) displayed higher levels of spontaneously released and microbiota-induced inflammatory mediators, including IL-6 and TGF-b, and surface adhesion molecules, than SCs isolated from healthy intestine (Normal SCs). Comparative transcriptome analysis confirmed the predominance of upregulated inflammatory response and cytokine signaling genes and pathway molecules in Crohn’s SCs. Importantly, intestinal SCs provided retinoic acid (RA), which regulated DC maturation, and in an in vitro cross-talk system E. coli LF82-stimulated Crohn’s SCs promoted differentiation of more inflammatory TNFhi/IL-12lo/RAlo DCs and IFN-ghi/IL-17hi effector T cells than Normal SCs. Explaining this finding, Crohn’s SCs synthesized less RA and expressed more retinaldehyde reductase DHRS3, which inhibits retinol conversion to retinal, than Normal SCs. Our findings uncover microbe-SC crosstalk in which mucosal SCs initiate and perpetuate DC-driven T-cell-mediated inflammation in Crohn’s disease.

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Glutamine addicted myeloma cells inhibits osteoblastic differentiation of bone marrow mesenchymal stromal cells limiting asparagine availability.

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

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Cellular retinoic acid binding protein 2 (CRABP2) inhibits tumor growth by two distinct mechanisms

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Cellular retinoic acid binding protein 2 (CRABP2) inhibits tumor growth by two distinct mechanisms

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