The relevance of the chemokine receptor ACKR3/CXCR7 on CXCL12-mediated effects in cancers with a focus on virus-related cancers

Cytokine Growth Factor Rev. 2014 Jun;25(3):307-16. doi: 10.1016/j.cytogfr.2014.04.006. Epub 2014 May 9.


Recent studies have highlighted the importance of understanding the molecular determinants of CXCL12-mediated effects in cancers. Once previously thought to interact exclusively with CXCR4, CXCL12 also binds with high affinity to CXCR7 (recently renamed ACKR3), which belongs to an atypical chemokine receptor family whose members fail to activate Gαi proteins but interact with β-arrestins. In addition to its capacity to control CXCL12 bioavailability, ACKR3 can either enhance or dampen CXCR4-mediated signaling and activity. In light of the most recent findings, we have examined the role of ACKR3 in cancer, including a subset of virus-related cancers.

Keywords: ACKR3/CXCR7; CXCL12/SDF-1; CXCR4; Cancer; Virus.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Arrestin / metabolism
  • Chemokine CXCL12 / metabolism*
  • GTP-Binding Protein alpha Subunits
  • Humans
  • Neoplasm Proteins / metabolism*
  • Neoplasms / metabolism*
  • Neoplasms / pathology
  • Neoplasms / virology
  • Receptors, CXCR / metabolism*
  • Receptors, CXCR4 / metabolism
  • Signal Transduction*
  • Tumor Virus Infections / metabolism*
  • Tumor Virus Infections / pathology


  • ACKR3 protein, human
  • Arrestin
  • CXCL12 protein, human
  • CXCR4 protein, human
  • Chemokine CXCL12
  • GTP-Binding Protein alpha Subunits
  • Neoplasm Proteins
  • Receptors, CXCR
  • Receptors, CXCR4