# ACKR3

Source: https://onco.cc/targets/ackr3/  
OnCo record `ackr3` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

ACKR3 (Atypical chemokine receptor 3) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Ovarian cancer, Colorectal cancer, Skin cancer and 1 more.

## Summary

Atypical chemokine receptor that controls chemokine levels and localisation via high-affinity chemokine binding that is uncoupled from classic ligand-driven signal transduction cascades, resulting instead in chemokine sequestration, degradation, or transcytosis. Also known as interceptor (internalising receptor) or chemokine-scavenging receptor or chemokine decoy receptor. Acts as a receptor for chemokines CXCL11 and CXCL12/SDF1.

Open Targets scores its association with cancer at 0.68 (direct and indirect evidence; datatypes literature 0.99, animal model 0.63, genetic association 0.45, somatic mutation 0.96). IntOGen calls it a driver in 1 cohort (1 activating, 0 loss-of-function), covering Ovarian Epithelial Tumour.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: atypical chemokine receptor 3; Atypical chemokine receptor 3; RDC1; GPR159; CMKOR1; CXCR7
- Tags: cancer-genes-wave
- Symbol: ACKR3
- Class: oncogene
- Biology: Atypical chemokine receptor that controls chemokine levels and localisation via high-affinity chemokine binding that is uncoupled from classic ligand-driven signal transduction cascades, resulting instead in chemokine sequestration, degradation, or transcytosis. Also known as interceptor (internalising receptor) or chemokine-scavenging receptor or chemokine decoy receptor. Acts as a receptor for chemokines CXCL11 and CXCL12/SDF1. Chemokine binding does not activate G protein-mediated signal transduction but instead induces beta-arrestin recruitment, leading to ligand internalisation and activation of MAPK signalling pathway. Required for regulation of CXCR4 protein levels in migrating interneurons, thereby adapting their chemokine responsiveness. In glioma cells, transduces signals via MEK/ERK pathway, mediating resistance to apoptosis. Location: Cell membrane; Early endosome; Recycling endosome (UniProt). Locus 2q37.3 (HGNC).
- Where found: Ovarian cancer: IntOGen driver in 1 cohort (OVT); Colorectal cancer: Open Targets association 0.54 with colorectal cancer (MONDO_0005575); Skin cancer: Open Targets association 0.52 with skin cancer (MONDO_0002898); Melanoma: Open Targets association 0.52 with melanoma (MONDO_0005105)

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it an activating (Act) driver in 1 cohort. Evidence tier "cohort-driver" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:23692: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:23692
- UniProt P25106: https://www.uniprot.org/uniprotkb/P25106/entry
- NCBI Gene 57007: https://www.ncbi.nlm.nih.gov/gene/57007
- Ensembl ENSG00000144476: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000144476

## Connected records

- collections: [IntOGen](https://onco.cc/collections/intogen/), [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Colorectal cancer](https://onco.cc/cancers/colorectal/), [Melanoma](https://onco.cc/cancers/melanoma/), [Ovarian cancer](https://onco.cc/cancers/ovarian/), [Skin cancer (all types)](https://onco.cc/cancers/skin-cancer/)

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JSON: https://onco.cc/api/v1/entities/ackr3.json