Abstract
Atypical chemokine receptors have recently emerged as important molecular players in health and diseases; they affect chemokine availability and function and impact a multitude of pathophysiological events, including the tumorigenesis process. This family of atypical receptors comprises five members: ACKR1/DARC, ACKR2/D6, ACKR3/CXCR7, ACKR4/CCRL1, and ACKR5/CCRL2. This work evaluated the differential expression of these receptors in prostate cancer using quantitative PCR. Further evaluation of CCRL2 at the protein level confirmed its overexpression in a metastatic cell line and in malignant prostatic tissues from patients. CCRL2, a presumed member of the atypical chemokine receptor family, plays a key role in lung dendritic cell trafficking to peripheral lymph nodes. Recent studies have reported the expression of CCRL2 in different human cancer cell lines and tissues. However, its function and expression in prostate cancer has not been previously addressed.
Highlights
Chemokines are a group of structurally homologous chemotactic molecules that control cell migration and positioning throughout development, homeostasis, and inflammation[1–4]
Chemokine receptors fall into two phylogenetically related subgroups: a larger subgroup of G protein-coupled leukocyte chemotactic receptors and a smaller subgroup of atypical chemokine receptors (ACKRs) that do not signal through G proteins and lack chemotactic activity[6–10]
As mRNA for CC-motif receptor-like 2 (CCRL2) exhibited the most differential expression, it was chosen for further analysis at the protein level in the prostate cancer cell line PC-3 and the non-tumorigenic PWR1-E cells
Summary
Chemokines are a group of structurally homologous chemotactic molecules that control cell migration and positioning throughout development, homeostasis, and inflammation[1–4]. These molecules function by signaling through specific chemokine receptors, a group of ~20 rhodopsin-like seven-transmembrane-spanning receptors in humans and mice[5–6]. ACKRs affect chemokine availability and function, impacting a CLC number: R737.25, Document code: A The authors reported no conflict of interests.
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