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 in-vestigate 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.

Expression of ccrl2 inhibits tumor growth by concentrating chemerin and inhibiting neoangiogenesis / Delbany, D. A.; Robert, V.; Dubois-vedrenne, I.; Del Prete, A.; Vernimmen, M.; Radi, A.; Lefort, A.; Libert, F.; Wittamer, V.; Sozzani, S.; Parmentier, M.. - In: CANCERS. - ISSN 2072-6694. - 13:19(2021). [10.3390/cancers13195000]

Expression of ccrl2 inhibits tumor growth by concentrating chemerin and inhibiting neoangiogenesis

Sozzani S.
Penultimo
Writing – Original Draft Preparation
;
2021

Abstract

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 in-vestigate 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.
2021
chemerin; chemR23; CMKLR1; rarres2; tumor angiogenesis
01 Pubblicazione su rivista::01a Articolo in rivista
Expression of ccrl2 inhibits tumor growth by concentrating chemerin and inhibiting neoangiogenesis / Delbany, D. A.; Robert, V.; Dubois-vedrenne, I.; Del Prete, A.; Vernimmen, M.; Radi, A.; Lefort, A.; Libert, F.; Wittamer, V.; Sozzani, S.; Parmentier, M.. - In: CANCERS. - ISSN 2072-6694. - 13:19(2021). [10.3390/cancers13195000]
File allegati a questo prodotto
File Dimensione Formato  
AlDelbany_Expression_2021.pdf

accesso aperto

Tipologia: Versione editoriale (versione pubblicata con il layout dell'editore)
Licenza: Creative commons
Dimensione 9.6 MB
Formato Adobe PDF
9.6 MB Adobe PDF

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1613612
Citazioni
  • ???jsp.display-item.citation.pmc??? 4
  • Scopus 11
  • ???jsp.display-item.citation.isi??? 10
social impact