Blood Res 2015; 50(4):
Published online December 31, 2015
https://doi.org/10.5045/br.2015.50.4.218
© The Korean Society of Hematology
1Department of Drug Activity, New Drug Development Center, Medical Innovation Foundation, Osong, Daejeon, Korea.
2Department of Internal Medicine, School of Medicine, Chungnam National University, Daejeon, Korea.
Correspondence to : Correspondence to Deog-Yeon Jo, M.D., Ph.D. Division of Hematology/Oncology, Department of Internal Medicine, Chungnam National University Hospital, 282 Munhwa-ro, Jung-gu, Daejeon 35015, Korea. Tel: +82-42-280-7162, deogyeon@cnu.ac.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
The 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
All 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 is involved in the regulation of autocrine CXCL12 in AML cells.
Keywords Acute myeloid leukemia, Apoptosis, Cell proliferation, Stromal cell-derived factor-1, CXCL12, CXCR7
Blood Res 2015; 50(4): 218-226
Published online December 31, 2015 https://doi.org/10.5045/br.2015.50.4.218
Copyright © The Korean Society of Hematology.
Ha-Yon Kim1, So-Yeon Lee2, Deog-Young Kim2, Ji-Young Moon2, Yoon-Seok Choi2, Ik-Chan Song2, Hyo-Jin Lee2, Hwan-Jung Yun2, Samyong Kim2, and Deog-Yeon Jo2*
1Department of Drug Activity, New Drug Development Center, Medical Innovation Foundation, Osong, Daejeon, Korea.
2Department of Internal Medicine, School of Medicine, Chungnam National University, Daejeon, Korea.
Correspondence to:Correspondence to Deog-Yeon Jo, M.D., Ph.D. Division of Hematology/Oncology, Department of Internal Medicine, Chungnam National University Hospital, 282 Munhwa-ro, Jung-gu, Daejeon 35015, Korea. Tel: +82-42-280-7162, deogyeon@cnu.ac.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
The 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
All 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 is involved in the regulation of autocrine CXCL12 in AML cells.
Keywords: Acute myeloid leukemia, Apoptosis, Cell proliferation, Stromal cell-derived factor-1, CXCL12, CXCR7
Acute myeloid leukemia (AML) cells express and produce C-X-C chemokine receptor 7 (CXCR7). (
Abbreviations: CXCL12, C-X-C motif ligand 12; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.
C-X-C motif ligand 12 (CXCL12) induces internalization of cell surface C-X-C chemokine receptor 7 (CXCR7) in acute myeloid leukemia (AML) cells. Flow cytometric analysis for cell surface CXCR7 in U937 cells before and after a 2-hr incubation with CXCL12 (200 ng/mL).
Cytokines and hypoxia do not alter C-X-C chemokine receptor 7 (CXCR7) expression in acute myeloid leukemia (AML) cells. (
Abbreviations: IL-6, interleukin 6; GM-SCF, granulocyte-macrophage colony-stimulating factor; TGF-β, tumor growth factor-β; INF-γ, interferon-γ; TNF-α, tumor necrosis factor-α; G-CSF, granulocyte colony-stimulating factor; SCF, stem cell factor; TPO, thrombopoietin; Con, control.
C-X-C chemokine receptor 7 (CXCR7) does not affect migration, serum-deprivation-induced apoptosis, or spontaneous proliferation of acute myeloid leukemia (AML) cells. Using small interfering RNA (siRNA) technology,
Knock-down of C-X-C chemokine receptor 7 (CXCR7) upregulates C-X-C motif ligand 12 (CXCL12) expression in acute myeloid leukemia (AML) cells. Using small interfering RNA (siRNA) technology,
Ha-Yon Kim, Ji-Young Hwang, Yoon-Suk Oh, Seong-Woo Kim, Hyo-Jin Lee, Hwan-Jung Yun, Samyong Kim, Young-Jun Yang, and Deog-Yeon Jo
Korean J Hematol 2011; 46(4): 244-252Seong Woo Kim, Jin Hee Hwang, Seon Ah Jin, Gak Won Yun, Young Joon Yang, Nam Whan Park, Hyo Jin Lee, Hwan Jung Yun, Deog Yeon Jo, Samyong Kim
Korean J Hematol 2007; 42(1): 24-32Sahar Jalilivand, Maryam Nabigol, Mehdi Bakhtiyaridovvombaygi and Ahmad Gharehbaghian
Blood Res 2024; 59():
Acute myeloid leukemia (AML) cells express and produce C-X-C chemokine receptor 7 (CXCR7). (
Abbreviations: CXCL12, C-X-C motif ligand 12; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.
|@|~(^,^)~|@|C-X-C motif ligand 12 (CXCL12) induces internalization of cell surface C-X-C chemokine receptor 7 (CXCR7) in acute myeloid leukemia (AML) cells. Flow cytometric analysis for cell surface CXCR7 in U937 cells before and after a 2-hr incubation with CXCL12 (200 ng/mL).
|@|~(^,^)~|@|Cytokines and hypoxia do not alter C-X-C chemokine receptor 7 (CXCR7) expression in acute myeloid leukemia (AML) cells. (
Abbreviations: IL-6, interleukin 6; GM-SCF, granulocyte-macrophage colony-stimulating factor; TGF-β, tumor growth factor-β; INF-γ, interferon-γ; TNF-α, tumor necrosis factor-α; G-CSF, granulocyte colony-stimulating factor; SCF, stem cell factor; TPO, thrombopoietin; Con, control.
|@|~(^,^)~|@|C-X-C chemokine receptor 7 (CXCR7) does not affect migration, serum-deprivation-induced apoptosis, or spontaneous proliferation of acute myeloid leukemia (AML) cells. Using small interfering RNA (siRNA) technology,
Knock-down of C-X-C chemokine receptor 7 (CXCR7) upregulates C-X-C motif ligand 12 (CXCL12) expression in acute myeloid leukemia (AML) cells. Using small interfering RNA (siRNA) technology,