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

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

PROVIDER: PRJNA762327 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15843312_1.fastq.gz	Fastqsanger.gz
	SRR15843312_2.fastq.gz	Fastqsanger.gz
	SRR15843313_1.fastq.gz	Fastqsanger.gz
	SRR15843313_2.fastq.gz	Fastqsanger.gz
	SRR15843314_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Expression of CCRL2 Inhibits Tumor Growth by Concentrating Chemerin and Inhibiting Neoangiogenesis.

Project description:CCRL2 belongs to the G protein-coupled receptor family and is one of the three chemerin receptors. It is considered as a non-signaling receptor, presenting chemerin to cells expressing the functional chemerin receptor ChemR23/CMKLR1 and possibly GPR1. In the present work, we investigate the role played by CCRL2 in mouse cancer models. Loss of function of Ccrl2 accelerated the development of papillomas in a chemical model of skin carcinogenesis (DMBA/TPA), whereas the growth of B16 and LLC tumor cell grafts was delayed. Delayed tumor growth was also observed when B16 and LLC cells overexpress CCRL2, while knockout of Ccrl2 in tumor cells reversed the consequences of Ccrl2 knockout in the host. The phenotypes associated with CCRL2 gain or loss of function were largely abrogated by knocking out the chemerin or Cmklr1 genes. Cells harboring CCRL2 could concentrate bioactive chemerin and promote the activation of CMKLR1-expressing cells. A reduction of neoangiogenesis was observed in tumor grafts expressing CCRL2, mimicking the phenotype of chemerin-expressing tumors. This study demonstrates that CCRL2 shares functional similarities with the family of atypical chemokine receptors (ACKRs). Its expression by tumor cells can significantly tune the effects of the chemerin/CMKLR1 system and act as a negative regulator of tumorigenesis.

| S-EPMC8508266 | biostudies-literature

Chemerin inhibits cancer progression by impairing the maturation of neovessels

Project description: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.

2019-05-05 | GSE98672 | GEO

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.

2023-08-04 | GSE212088 | GEO

Chemerin attenuates acute kidney injury by inhibiting ferroptosis via the AMPK/NRF2/SLC7A11 axis

Project description:Acute kidney injury (AKI) is a common and life-threatening condition associated with cell death, where ferroptosis plays a critical role. Chemerin, primarily produced in white adipose tissue, has multiple biological functions in renal pathophysiology. However, to date, whether and how chemerin regulates the progression of AKI remain unclear. Here, we found that chemerin expression was reduced in both AKI model mice and cells. Similarly, serum chemerin levels were also decreased in AKI patients. The administration of recombinant chemerin improves renal function in ischemia-reperfusion (I/R) model mice. Chemerin significantly attenuates ferroptosis in kidneys. In TCMK-1 cells, chemerin knockdown further aggravates ferroptosis. Mechanistically, chemerin activates AMP-activated protein kinase (AMPK), which induces the phosphorylation of nuclear factor erythroid 2-related factor 2 (NRF2) in renal tubular cells. Subsequently, NRF2 translocates into the nucleus, where it stimulates the expression of cystine/glutamate antiporter solute carrier (SLC7A11). As a result, cystine uptake and glutathione (GSH) biosynthesis in renal tubular cells were increased, which confers cells with higher capacity against ferroptosis. Overall, our findings indicate that chemerin plays a protective role in AKI by repressing ferroptosis in renal tubular cells, which is likely due to the activation in the AMPK/NRF2/SLC7A11 axis.

2024-12-01 | GSE283126 | GEO

The role of chemerin in clear cell renal cell carcinoma

Project description:The most common subset of renal carcinoma, clear cell renal cell carcinoma (ccRCC), is characterized by accentuated accumulation of neutral lipids in lipid droplets and adipogenic trans-differentiation. Because obesity is a major risk factor in the development of ccRCC, we investigated the role of the adipokines in driving lipid metabolism and tumorigenesis in ccRCC. Through in silico screening, we identified the adipokine chemerin as candidate pro-oncogenic factor that is overexpressed in tumors and prognostic for patient outcome. Both ccRCC patient tumor tissues and serum exhibit elevated chemerin levels as compared to normal controls in an obesity-dependent manner. Attenuation of chemerin by several approaches in ccRCC cells led to significant impairments of tumor growth in both in vitro and in vivo models. A multi-omic approach revealed that chemerin suppresses fatty acid oxidation and maintains fatty acid levels which feed into transcriptional activation of hypoxia-inducible factor 2 (HIF2) expression. Suppression of chemerin therefore induced excess fatty acid oxidation and led to ferroptosis. CoQ and mitochondrial complex IV, derived mainly from lipid, were affected after chemerin inhibition, contributing to mitochondrial dysfunction and lipid reactive oxygen species production. Monoclonal antibody targeting chemerin led to reduced lipid storage, increased cell death, and diminished tumor growth, strengthening the translational potential of chemerin inhibition. Collectively, the results suggest that obesity and tumor cells contribute to ccRCC through the expression of chemerin, which is indispensable in ccRCC biology.

2021-08-11 | GSE159716 | GEO

Exploring CCRL2 chemerin binding using accelerated molecular dynamics.

Project description:Chemokine (C-C motif) receptor-like 2 (CCRL2), is a seven transmembrane receptor closely related to the chemokine receptors CCR1, CCR2, CCR3, and CCR5. Nevertheless, CCRL2 is unable to activate conventional G-protein dependent signaling and to induce cell directional migration. The only commonly accepted CCRL2 ligand is the nonchemokine chemotactic protein chemerin (RARRES2). The chemerin binding to CCLR2 does induce leukocyte chemotaxis, yet, genetic targeting of CCRL2 was shown to modulate the inflammatory response in different experimental models. This mechanism was shown to be crucial for lung dendritic cell migration, neutrophil recruitment, and Natural Killer cell-dependent immune surveillance in lung cancer. To gain more insight in the interactions involved in the CCRL2-chemerin, the binding complexes were generated by protein-protein docking, then submitted to accelerated molecular dynamics. The obtained trajectories were inspected by principal component analyses followed by kernel density estimation to identify the ligand-receptor regions most frequently involved in the binding. To conclude, the reported analyses led to the identification of the putative hot-spot residues involved in CCRL2-chemerin binding.

| S-EPMC9543397 | biostudies-literature

Effect of chemerin in primary human hepatocytes (PHH) and hepatic stellate cells (HSC)

Project description:Effect of chemerin in these cells is hardly known. Cells of three donors were used to identify genes regulated by the active chemerin isoform.

2022-07-06 | GSE156698 | GEO

Chemerin attenuates acute kidney injury by inhibiting ferroptosis via the AMPK/NRF2/SLC7A11 axis

Project description:Chemerin attenuates acute kidney injury by inhibiting ferroptosis via the AMPK/NRF2/SLC7A11 axis

| PRJNA1192208 | ENA

Chemerin triggers migration of a CD8 T cell subset with natural killer cell functions

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.

2024-05-01 | GSE219255 | GEO

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