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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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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

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

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

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

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

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

The impact of chemerin on transcriptomic profile of swine luteal cells during mid-luteal phase of estrous cycle

Project description:The aim of the study was to investigate the influence of chemerin on the transcriptomic profile of porcine in vitro cultured luteal cells collected during the mid-luteal phase of estrous cycle.

2022-02-20 | E-MTAB-11434 | biostudies-arrayexpress

YAP targets TEAD-NF-κB complex and inhibits ccRCC tumor growth

Project description:YAP targets TEAD-NF-κB complex and inhibits ccRCC tumor growth

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