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Chemerin inhibits cancer progression by impairing the maturation of neovessels

ABSTRACT: Chemerin is a leukocyte chemoattractant and an adipokine. Overexpression of chemerin by tumor cells or the host inhibits tumor progression in different mouse models, through a mechanism involving the chemerin receptor CMKLR1 and impairment of endothelial cell/pericyte interactions in neovessels.

ORGANISM(S): Mus musculus

PROVIDER: GSE98672 | GEO | 2019/05/05

REPOSITORIES: GEO

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Expression of CCRL2 inhibits tumor growth by concentrating chemerin and inhibiting neoangiogenesis

Project description:CCRL2 is a non-signaling G protein-coupled receptor for chemerin, a leukocyte chemoattractant and an adipokine. Graft of B16 melanoma or Lewis lung carcinoma (LLC) cell lines in CCRL2 KO mice results in delayed growth of the tumors.

2021-10-20 | GSE183914 | GEO

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2024-04-11 | E-MTAB-14016 | biostudies-arrayexpress

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Project description:We identified subsets of human CD28- effector CD8 T cells, of CCR7- CD45RO+ effector memory (EM) and CCR7- CD45RO- effector memory RA (EMRA) phenotypes, that express the chemerin receptor CMKLR1 and bind chemerin via the receptor. This study investigates differential gene expression between the chemerin binding and nonbinding human CD8 EMRA T cell subsets.

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The role of chemerin in clear cell renal cell carcinoma

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2021-08-11 | GSE159716 | GEO

Adipokine chemerin impairs the receptive and metabolic functions of endometrial epithelial cells revealed by transcriptomic analysis

Project description:Endometrium, the lining of the uterus, changes dynamically in response to fluctuations in ovarian hormones. The proper endocrine environment regulates endometrial functions: menstruation and supporting pregnancy. Obesity is closely related to endometrial dysfunction, which seriously affects women's health and fertility, but the pathological mechanism is unknown. Chemerin is an adipokine involved in multiple biological events such as immunity and metabolism by acting on its functional receptors. This study aimed to characterize the effects of chemerin on human endometrial epithelial cells by RNA-Seq.

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RNA-seq of intestinal epithelial cells isolated from DSS colitis model mice

Project description:In the present study, we demonstrated that mice deficient in chemerin or IEC-specific CMKLR1 expression were highly susceptible to DSS-induced colitis and subsequent tumorigenesis, which was reversed by suppressing colonic neutrophilic inflammation using CXCR2 inhibitor. Surprisingly, we found that lack of the Chemerin-CMKLR1 signaling specifically reduced colonic epithelial expression of lactoperoxidase (LPO), an epithelial peroxidase which could utilize H2O2 to oxidase thiocyanates to antibiotic compound (Bafort et al., 2014). Importantly, we demonstrated that impaired epithelial LPO expression accounted for outgrowth of potentially pathogenic Gram-negative bacteria following epithelial injury, which led to overproduction of CXCL1/2 and pathological neutrophilic inflammation in mice with epithelial Chemerin-CMKLR1 signaling deficiency. Finally, lack of epithelial Chemerin-CMKLR1 signaling impaired early host defense against enteric bacteria, which was reversed by LPO supplementation. Taken together, our study uncovers a critical role of epithelial Chemerin-CMKLR1 signaling in restricting pathological colonic neutrophilia via potentiating LPO-mediated epithelial innate defense, thereby rendering protection against microbiota-driven colitis and tumorigenesis.

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RNA-seq of cold stimulated inguinal fat of wild type and Rarres2-/- mice

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CCRL2 expression by specialized lung capillary endothelial cells controls NK cells homing in lung cancer

Project description:Patterns of chemotactic receptors regulate the homing of leukocytes to tissues. Here we report that the CCRL2/chemerin/CMKLR1 axis represent a selective pathway for the homing of NK cells to the lung. CCRL2 is a non-signaling seven-transmembrane domain receptor able to control lung tumor growth. Total or endothelial cell targeted CCRL2 deletion or the deletion of its ligand chemerin were found to promote tumor progression in a KrasG12D/+;p53LoxP lung cancer model. This phenotype was dependent on the reduced recruitment of CD27-CD11b+ mature NK cells. Mining scRNA-seq databases identified CCRL2 expression as the hallmark of general alveolar lung capillary endothelial cells (gCaps). CCRL2 expression is epigenetically regulated in lung endothelium. In vivo administration of low doses of the demethylating agent 5-Aza induced CCRL2 upregulation, increased recruitment of NK cells and lung protection in a tumor model. These results identify CCRL2 as a NK cell lung homing molecule that might be exploited to promote NK cell-mediated lung immune surveillance.

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