Abstract
Recently, a novel CXCL12-binding receptor, has been identified. This CXCL12-binding receptor commonly known as CXCR7 (CXC chemokine receptor 7), has lately, based on a novel nomenclature, has received the name ACKR3 (atypical chemokine receptor 3). In this study, we aimed to investigate the expression of CXCR7 in leukemic cells, as well as its participation in CXCL12 response. Interesting, we clearly demonstrated that CXCR7 is highly expressed in acute lymphoid leukemic cells compared with myeloid or normal hematopoietic cells and that CXCR7 contributed to T-acute lymphoid leukemic cell migration induced by CXCL12. Moreover, we showed that the cellular location of CXCR7 varied among T-lymphoid cells and this finding may be related to their migration capacity. Finally, we hypothesized that CXCR7 potentiates CXCR4 response and may contribute to the maintenance of leukemia by initiating cell recruitment to bone marrow niches that were once occupied by normal hematopoietic stem cells.
Highlights
Chemokine receptors belong to the superfamily of heptahelical G protein-coupled receptors (GPCRs) and are involved in a vast array of physiological events [1,2,3]
Previous studies have shown a significant correlation between chemokine receptor status in human cancers and prognosis and/or metastases in a variety of malignant tumors such as T-cell leukemia (CCR4), hepatocellular carcinoma (CCR6), gastric carcinoma (CCR7), renal cell carcinoma (CXCR3), ovarian cancer (CXCR4), osteosarcoma (CXCR4), colorectal cancer (CCR7 and CXCR4), and malignant melanoma (CXCR3 and CXCR4) [22]
In this report we investigated the expression of the novel chemokine receptor CXCR7 in myelodysplastic syndromes and acute leukemias
Summary
Chemokine receptors belong to the superfamily of heptahelical G protein-coupled receptors (GPCRs) and are involved in a vast array of physiological events [1,2,3]. Given that bone marrow (BM) stromal cells are major producers of CXCL12 [17,18] and that CXCR4 expression is thought to be higher in BM-residing blasts than in circulating blasts, CXCL12/CXCR4 interactions are likely to facilitate the retention of blasts in the BM [18,19]. Direct signaling and/or chemokine responses of CXCL12 and CXCL11 through CXCR7 have been shown to be b-arrestin protein coupled and to activate kinase phosphorylation, leading to increased motility and chemotaxis [23,26,38]
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