ArticleBlood research2015
Expression and functional roles of the chemokine receptor CXCR7 in acute myeloid leukemia cells.
Article in Blood research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Review
- CXCR4 as a therapeutic target in acute myeloid leukemia.Leukemia · 2024Review
- ACKR3 promotes CXCL12/CXCR4-mediated cell-to-cell-induced lymphoma migration through LTB4 production.Frontiers in immunology · 2022Article
- The Effect of Hypoxia on the Expression of CXC Chemokines and CXC Chemokine Receptors-A Review of Literature.International journal of molecular sciences · 2021Review
- CXCR7: a β-arrestin-biased receptor that potentiates cell migration and recruits β-arrestin2 exclusively through Gβγ subunits and GRK2.Cell & bioscience · 2020Article
- Expression and regulation effects of chemokine receptor 7 in colon cancer cells.Oncology letters · 2020Article
- The Role of Selected Chemokines and Their Receptors in the Development of Gliomas.International journal of molecular sciences · 2020Review
- Leukemia Stem Cell Release From the Stem Cell Niche to Treat Acute Myeloid Leukemia.Frontiers in cell and developmental biology · 2020Review
- Risk Stratification in Acute Myeloid Leukemia Using CXCR Gene Signatures: A Bioinformatics Analysis.Frontiers in oncology · 2020Article
- CXCR7 participates in CXCL12-mediated migration and homing of leukemic and normal hematopoietic cells.Stem cell research & therapy · 2018Article
- ACKR3 expression on diffuse large B cell lymphoma is required for tumor spreading and tissue infiltration.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe C-X-C chemokine receptor 7 (CXCR7) has been shown to be a decoy receptor for CXCR4 in certain cell types. We investigated the expression status and functional roles of CXCR7 in acute myeloid leukemia (AML) cells in vitro.
methodsCXCR7 mRNA was knocked down in AML cells by using small interfering RNA (siRNA) technology, and subsequent biological alterations in the cells were evaluated in vitro.
resultsAll AML cell lines examined in this study (U937, K562, KG1a, HL-60, and MO7e) and primary CD34(+) cells obtained from patients with AML expressed CXCR7 mRNA at various levels. Western blotting showed that all AML cells produced CXCR7. Furthermore, all AML cells expressed CXCR7 in both the cytoplasm and on the cell surface at various levels. Stromal cell-derived factor-1 (SDF-1; C-X-C motif ligand 12 (CXCL12)) induced internalization of cell surface CXCR7. However, neither hypoxia nor the examined hematopoietic growth factors (interleukin-1β (IL-1β), IL-3, IL-6, granulocyte-colony-stimulating factor, granulocyte, macrophage-colony-stimulating factor, and stem cell factor) and proinflammatory cytokines (interferon-γ, transforming growth factor-β, and tumor necrosis factor-α) were found to alter cell surface CXCR7 expression. The transfection of AML cells with CXCR4 siRNA, but not CXCR7 siRNA, significantly impaired the CXCL12-induced transmigration of the cells. The transfection of AML cells with CXCR7 siRNA did not affect the survival or proliferation of these cells. Knockdown of CXCR7, but not CXCR4, induced the upregulation of CXCL12 mRNA expression and CXCL12 production in AML cells.
conclusionCXCR7 is involved in the regulation of autocrine CXCL12 in AML cells.
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