CCR7 is involved in BCR-ABL/STAP-2-mediated cell growth in hematopoietic Ba/F3 cells

Kubo, Kaori; Iwakami, Masashi; Muromoto, Ryuta; Kitai, Yuichi; Kawa, Shigeyuki; Sekine, Yoshifumi; Oritani, Kenji; Matsuda, Tadashi

doi:10.1016/j.bbrc.2015.06.020

Cited by 5 publications

(4 citation statements)

References 23 publications

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“…Signal transducing adaptor protein-2 (STAP-2) binds to BCR-ABL leading to enhanced BCR-ABL phosphorylation and downstream signaling. STAP-2 binding to BCR-ABL also enhanced CCR7, CCL19 and CCL21 expression via the MAPK/ERK pathway and was required for BaF3 cell growth in vitro [ 281 ]. When injected into nude Balb/c mice, small hairpin RNA inhibitor of CCR7 led to decreased tumor size compared to control Ba/F3, suggesting that CCR7 is required for the STAP-2/BCR-ABL-induced CML growth [ 281 ].…”

Section: Bone and Blood Cancersmentioning

confidence: 99%

C-C Chemokine Receptor 7 in Cancer

Bill

Allen

Vines

2022

Cells

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C-C chemokine receptor 7 (CCR7) was one of the first two chemokine receptors that were found to be upregulated in breast cancers. Chemokine receptors promote chemotaxis of cells and tissue organization. Since under homeostatic conditions, CCR7 promotes migration of immune cells to lymph nodes, questions immediately arose regarding the ability of CCR7 to direct migration of cancer cells to lymph nodes. The literature since 2000 was examined to determine to what extent the expression of CCR7 in malignant tumors promoted migration to the lymph nodes. The data indicated that in different cancers, CCR7 plays distinct roles in directing cells to lymph nodes, the skin or to the central nervous system. In certain tumors, it may even serve a protective role. Future studies should focus on defining mechanisms that differentially regulate the unfavorable or beneficial role that CCR7 plays in cancer pathophysiology, to be able to improve outcomes in patients who harbor CCR7-positive cancers.

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Section: Bone and Blood Cancersmentioning

confidence: 99%

C-C Chemokine Receptor 7 in Cancer

Bill

Allen

Vines

2022

Cells

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“…Moreover, depressed CCR7 expression was associated with reduced migratory ability to its ligands, CCL19 and CCL21. On the contrary, Kubo et al observed that BCR-ABL cooperated with signal transducing adaptor protein (STAP)-2 to induce the expression of CCR7 and CXCR4 and the production of the ligands for CCR7, CCL19, and CCL21, in a murine hematopoietic BaF/3 cell [ 100 ], raising the possibility of the contribution of the CCR7 axis to CML cell proliferation. Hromas et al, however, claimed that CCR7 ligands, CCL19 and CCL21, and a CCR6 ligand, CCL20, inhibited proliferation of CML progenitor cells as well as normal progenitor cells [ 101 ].…”

Section: Resultsmentioning

confidence: 99%

Chemokines as a Conductor of Bone Marrow Microenvironment in Chronic Myeloid Leukemia

Mukaida

Tanabe

Baba

2017

IJMS

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All blood lineage cells are generated from hematopoietic stem cells (HSCs), which reside in bone marrow after birth. HSCs self-renew, proliferate, and differentiate into mature progeny under the control of local microenvironments including hematopoietic niche, which can deliver regulatory signals in the form of bound or secreted molecules and from physical cues such as oxygen tension and shear stress. Among these mediators, accumulating evidence indicates the potential involvement of several chemokines, particularly CXCL12, in the interaction between HSCs and bone marrow microenvironments. Fusion between breakpoint cluster region (BCR) and Abelson murine leukemia viral oncogene homolog (ABL)-1 gene gives rise to BCR-ABL protein with a constitutive tyrosine kinase activity and transforms HSCs and/or hematopoietic progenitor cells (HPCs) into disease-propagating leukemia stem cells (LSCs) in chronic myeloid leukemia (CML). LSCs can self-renew, proliferate, and differentiate under the influence of the signals delivered by bone marrow microenvironments including niche, as HSCs can. Thus, the interaction with bone marrow microenvironments is indispensable for the initiation, maintenance, and progression of CML. Moreover, the crosstalk between LSCs and bone marrow microenvironments can contribute to some instances of therapeutic resistance. Furthermore, evidence is accumulating to indicate the important roles of bone marrow microenvironment-derived chemokines. Hence, we will herein discuss the roles of chemokines in CML with a focus on bone marrow microenvironments.

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“…Chronic myeloid leukemia (CML) is a clonal disease characterized by premature release of aberrant cells from the BM alongside their substantial accumulation in PB, spleen, and BM (202). In CML, the presence of the Philadelphia chromosome and its oncogenic product, the fusion oncoprotein BCR/ABL, is directly linked to multiple pathways involved in cell survival, growth promotion, and disease progression (203,204). Similarly to LCH, an impaired adhesion and motility towards CCR7 was first reported for CML cells (14,205) though this effect remains controversial since more recent reports showed in vitro and in vivo how a positive activation loop between BCR-ABL and the signal-transducing adaptor protein-2 (STAP-2) led to enhanced ERK signaling resulting in overexpression of CCR7, LN enlargement, and hepatosplenomegaly (203,204).…”

Section: Myeloproliferative Disordersmentioning

confidence: 99%

“…In CML, the presence of the Philadelphia chromosome and its oncogenic product, the fusion oncoprotein BCR/ABL, is directly linked to multiple pathways involved in cell survival, growth promotion, and disease progression (203,204). Similarly to LCH, an impaired adhesion and motility towards CCR7 was first reported for CML cells (14,205) though this effect remains controversial since more recent reports showed in vitro and in vivo how a positive activation loop between BCR-ABL and the signal-transducing adaptor protein-2 (STAP-2) led to enhanced ERK signaling resulting in overexpression of CCR7, LN enlargement, and hepatosplenomegaly (203,204). Whether these contradictory outcomes are a result of differential in vitro versus in vivo settings, or a consequence of artifacts associated to the use of cell lines versus primary tumor cells, needs clarification.…”

Section: Myeloproliferative Disordersmentioning

confidence: 99%

CCR7 in Blood Cancers – Review of Its Pathophysiological Roles and the Potential as a Therapeutic Target

Cuesta-Mateos

Terrón²,

Herling³

2021

Front. Oncol.

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According to the classical paradigm, CCR7 is a homing chemokine receptor that grants normal lymphocytes access to secondary lymphoid tissues such as lymph nodes or spleen. As such, in most lymphoproliferative disorders, CCR7 expression correlates with nodal or spleen involvement. Nonetheless, recent evidence suggests that CCR7 is more than a facilitator of lymphatic spread of tumor cells. Here, we review published data to catalogue CCR7 expression across blood cancers and appraise which classical and novel roles are attributed to this receptor in the pathogenesis of specific hematologic neoplasms. We outline why novel therapeutic strategies targeting CCR7 might provide clinical benefits to patients with CCR7-positive hematopoietic tumors.

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CCR7 is involved in BCR-ABL/STAP-2-mediated cell growth in hematopoietic Ba/F3 cells

Cited by 5 publications

References 23 publications

C-C Chemokine Receptor 7 in Cancer

C-C Chemokine Receptor 7 in Cancer

Chemokines as a Conductor of Bone Marrow Microenvironment in Chronic Myeloid Leukemia

CCR7 in Blood Cancers – Review of Its Pathophysiological Roles and the Potential as a Therapeutic Target

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