Download Gene Section CCR1 (chemokine (C-C motif) receptor 1) in Oncology and Haematology

Atlas of Genetics and Cytogenetics
in Oncology and Haematology
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Gene Section
Review
CCR1 (chemokine (C-C motif) receptor 1)
Qiang Gao, Jia Fan
Liver Cancer Institute, Zhong Shan Hospital and Shanghai Medical School, Fudan University, Shanghai, P R
China (QG, JF)
Published in Atlas Database: April 2010
Online updated version : http://AtlasGeneticsOncology.org/Genes/CCR1ID44379ch3p21.html
DOI: 10.4267/2042/44930
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 2.0 France Licence.
© 2011 Atlas of Genetics and Cytogenetics in Oncology and Haematology
Description
Identity
Sequence length: 6633 bp; coding sequence: CDS 721139. 2 exons; number of SNPs: 97.
Other names: CD191, CKR-1, CKR1, CMKBR1,
HM145, MIP1aR, SCYAR1
HGNC (Hugo): CCR1
Location: 3p21.31
Transcription
2690 bp mRNA, no alternative splicing.
Pseudogene
DNA/RNA
No pseudogenes have been reported for CCR1.
Note
CCR1, a member of the beta chemokine receptor
family, is a seven transmembrane protein similar to G
protein-coupled receptors. CCR1 is the first human CC
chemokine receptor to be identified at the cDNA level.
It has a functional viral homolog, US28, which is a
human cytomegalovirus.The ligands of this receptor
include macrophage inflammatory protein 1 alpha
(MIP-1 alpha), regulated on activation normal T
expressed and secreted protein (RANTES), monocyte
chemoattractant protein 3 (MCP-3), and myeloid
progenitor inhibitory factor-1 (MPIF-1). This gene and
other chemokine receptor genes, including CCR2,
CCRL2, CCR3, CCR5 and CCXCR1, form a gene
cluster on chromosome 3p.
Atlas Genet Cytogenet Oncol Haematol. 2011; 15(1)
Protein
Note
Chemokine receptors are cytokine receptors found on
the surface of certain cells, which interact with a type
of cytokine called a chemokine. They each have a 7
transmembrane structure and couple to G-protein for
signal transduction within a cell, making them
members of a large protein family of G protein-coupled
receptors. Following interaction with their specific
chemokine ligands, chemokine receptors trigger a flux
in intracellular calcium (Ca2+) ions (calcium signaling).
This causes cell responses, including the onset of a
process known as chemotaxis that traffics the cell to a
desired location within the organism.
1
CCR1 (chemokine (C-C motif) receptor 1)
Gao Q, Fan J
Predicted structure and amino acid sequence of CCR1. The typical serpentine structure is depicted with three extracellular (top) and
three intracellular (bottom) loops and seven transmembrane domains. The shaded horizontal band represents the cell membrane. Amino
acids are listed with a single letter code.
Chemokine receptors share many common structural
features; they are composed of about 350 amino acids
that are divided into a short and acidic N-terminal end,
seven helical transmembrane domains with three
intracellular and three extracellular hydrophilic loops,
and an intracellular C-terminus containing serine and
threonine residues that act as phosphorylation sites
during receptor regulation. The first two extracellular
loops of chemokine receptors are linked together by
disulfide bonding between two conserved cysteine
residues. The N-terminal end of a chemokine receptor
binds to chemokine(s) and is important for ligand
specificity. G-proteins couple to the C-terminal end,
which is important for receptor signaling following
ligand binding.
lymphocytes; blood derived mast cells, dendritic cells,
basophils and eosinophils; bone marrow stromal cells;
microvascular endothelial cells; vascular smooth
muscle cells.
Localisation
Cell membrane; multi-pass membrane protein.
Function
Receptor for a C-C type chemokine. Binds to CCL3
(MIP-1-alpha), CCL5 (RANTES), CCL7 (MCP-3),
CCL9 (MIP-1-gamma), CCL14 (HCC-1), CCL15
(MIP-1-delta), CCL16 (HCC-4) and CCL23 (MIP-3),
and, less efficiently, to MIP-1-beta or MCP-1 and
subsequently transduces a signal by increasing the
intracellular calcium ions level. The major function of
CCR1 is to regulate leukocyte trafficking in
hematopoiesis and in innate and adaptive immunity.
Other functions include angiogenic activity,
ischemia/reperfusion
injury,
immune-cell
differentiation, phagocyte activation, and affecting
stem cell proliferation.
Description
355 amino acids; 41173 Da.
Expression
Monocyte/macrophages; T cells; platelets; tonsil B
Atlas Genet Cytogenet Oncol Haematol. 2011; 15(1)
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CCR1 (chemokine (C-C motif) receptor 1)
Gao Q, Fan J
ligands, RANTES and MIP-1alpha, respectively, were
demonstrated in MM cell lines and primary MM cells.
Osteoclasts (OCL) secrete high levels of CCL3 and
MM cells the express CCR1, the interaction between
which plays a key role in the pathogenesis of MMrelated osteolytic bone disease. Through CCL3-CCR1
axis OCL cells promote OCL formation and, in turn,
OCL enhance MM cell proliferation.
In murine models of MM, MIP-1alpha, an OCL
stimulatory factor produced by primary MM cells,
increases bone destruction and tumor burden, by
interacting with chemokine receptors CCR1 and CCR5
that widely expressed in human OCL precursors,
myeloma cell lines, and purified marrow plasma cells
from MM patients. Neutralizing antibodies to CCR1 or
CCR5 inhibited MIP-1alpha-induced OCL formation.
Furthermore, MCP-3, which binds CCR1 but not
CCR5, and the CCR1-specific antagonist, BX471,
markedly inhibited OCL formation stimulated with
MIP-1alpha. Anti-CCR1, anti-CCR5, or BX471 also
inhibited the upregulation of beta1 integrin myeloma
cells induced by MIP-1alpha, as well as the adherence
of myeloma cells to stromal cells and IL-6 production
by stromal cells in response to myeloma cells.
The oncogene c-maf is translocated in approximately
5%-10% of MM. By gene expression profiling, three cmaf target genes, cyclin D2, integrin beta7 and CCR1,
were identified.
Homology
CCR1 protein contains considerable amino acid
sequence homology to other C-C chemokines: CCR2B
(56%), CCR3 (54%), CCR4 (49%), CCR5 (55%).
Implicated in
Hematolymphoid neoplasia
Prognosis
CCR1 expression correlates with overall survival in the
non-germinal center subtype of diffuse large B-cell
lymphoma. In follicular lymphoma, high levels of
CCR1 are associated with a shorter survival interval,
and CCR1 is a marker of an immune switch between
macrophages and a T cell-dominant response.
Oncogenesis
CCR1 is expressed in intraepithelial B cells of human
tonsil and granulocytic/monocytic cells in the bone
marrow. Immunohistochemical analysis of 944 cases of
hematolymphoid neoplasia identified CCR1 expression
in a subset of B- and T-cell lymphomas, plasma cell
myeloma, acute myeloid leukemia, and classical
Hodgkin lymphoma. In 13 patients with chronic
lymphocytic leukemia (CLL), 9 with hairy cell
leukemia (HCL), 5 with mantle cell lymphoma (MCL),
5 with marginal zone B-cell lymphoma (MZL), 6 with
small lymphocytic lymphoma (SLL), and 5 with
follicular cell lymphoma (FCL), flow cytometry
analysis demonstrated that CCR1 was expressed in
70% of patients with CLL and 40% of those with HCL
but was lacking in patients with MCL, MZL, SLL, and
circulating normal B cells.
Circulating CD3+ T cells derived from healthy
individuals and acute myelogenous leukemia patients
with therapy-induced cytopenia after conventional
chemotherapy or allogeneic stem cell transplantation
showed no qualitative differences in CCR1 expression,
that is, low expression for all the three groups.
Hepatocellular carcinoma
Oncogenesis
Hepatic myofibroblast LI90 cells express and secrete
MCP-1/CCL2. Through its receptors CCR1 and CCR2
as well, LI90 induces human hepatocellular carcinoma
(HCC) Huh7 cell migration and invasion, which are
strongly inhibited by heparin, beta-D-xyloside and antisyndecan-1 and -4 antibodies. RANTES/CCL5 strongly
stimulates the migration and the invasion of Huh7 cells
by stimulating the tyrosine phosphorylation of focal
adhesion kinase as well as activating matrix
metalloproteinase-9, and to a lesser extent that of
Hep3B cells. The RANTES-induced migration and
invasion of Huh7 cells are also strongly inhibited by
anti-CCR1 antibodies and heparin, as well as by beta-dxyloside treatment of the cells, suggesting that CCR1
and glycosaminoglycans are involved in these events.
We found that the miRNA-mediated knockdown
expression of CCR1 significantly inhibited the invasive
ability of and reduced the secretion of MMP-2 in
hepatocellular carcinoma HCCLM3 cells, but only had
a minor effect on the cellular proliferation. CCR1
expression was also detected on primary HCC cells and
to a lesser degree, on endothelial cells in HCC tissues
but not in normal liver tissues. Similarly, CCL3
expression was detected in HCC cells, endothelial cells,
and to a lesser degree, fibroblast-like cells in HCC
tissue, whereas only occasional vascular endothelial
cells and inflammatory cells in normal liver tissues
were weakly positive for CCL3. IL-1 enhances the
Multiple myeloma
Prognosis
In 80 multiple myeloma (MM) patients with bone
marrow samples, patients with active disease showed a
significantly lower expression of CCR1, CCR2, as well
as CXCR4 than patients with non-active disease. This
chemokine receptor expression profile correlated with
serum beta2-microglobulin, C-reactive protein and
hemoglobin. Multivariate analysis identified the
chemokine receptor expression profile as an
independent prognostic factor.
Oncogenesis
Human MM cells express at least three different
chemokine receptors that are functionally involved in
MM cell migration, i.e. CCR1, CCR2 and CXCR4,
some also CCR6 and CXCR3. cDNA arrays identified
CCR1 and CCR2 are overexpressed in myeloma cells
compared to autologous B-lymphoblastoid cell lines.
The expression of CCR1 and the migration to their
Atlas Genet Cytogenet Oncol Haematol. 2011; 15(1)
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CCR1 (chemokine (C-C motif) receptor 1)
Gao Q, Fan J
local production of CCL3, which interact with CCR1
expressed on HCC cells, in an autocrine and/or
paracrine manner. In a murine HCC model, injected
tumor cells were transfected with HSV-thymidine
kinase gene and then treated with ganciclovir (GCV).
GCV treatment induced massive tumor cell apoptosis
accompanied with intratumoral CCR1+CCR5+
dendritic cell infiltration. Tumor-infiltrating T cells and
macrophages expressed CCL3, suggesting CCR1CCL3 play a crucial role in the regulation of
intratumoral dendritic cell accumulation and the
subsequent establishment of tumor immunity following
induction of tumor apoptosis by suicide genes. CCL3
and CCR1 are also expressed in 2 different models of
HCC, i.e., N-nitrosodiethylamine (DEN)-induced HCC
and HCC induced by hepatitis B virus. After DEN
treatment, tumor foci number and sizes were
remarkably reduced in CCR1- and CCL3-deficient
mice, comparing with wild-type (WT) mice. Also,
tumor angiogenesis markedly diminished, intratumoral
Kupffer cells number reduced, MMP9 gene expression
attenuated and MMP9+ cell numbers decreased in
CCL3- and CCR1-deficient mice, as compared with
WT mice. These observations suggest the contribution
of the CCR1-CCL3 axis to HCC progression.
Oral squamous cell carcinoma
Oncogenesis
Expression of CCL3 and CCR1 is significant higher in
oral squamous cell carcinoma compared with the
normal controls. The percentages of CCL3+ and
CCR1+ cells were observed to be similar in
parenchyma and stroma in cases without lymph node
metastasis when compared with lymph node metastasis
positive cases.
Ovarian cancer
Oncogenesis
mRNA for CCR1, -2a, -2b, -3, -4, -5, and -8 was
detected in cells from human ovarian cancer ascites.
Further, flowcytometry showed CD14+ macrophages
within ascites consistently expressed CCR1, -2, and -5,
and >60% of all T cells expressed CCR1. Although
ovarian
cancer
ascitic
and
blood
monocyte/macrophages express CCR1, they failed to
migrate in response to the RANTES. Compared with
that of normal blood, cell surface expression level for
CCR1 was higher in ascites. In a monocytic cell line in
vitro, CCR1 mRNA expression was increased 5-fold by
hypoxia. In 25 patients with ovarian cancer, CCR1 was
detected in samples from 75% of patients, where CCR1
localised to macrophages and lymphocytes, and there
was a correlation between numbers of CD8+ cells and
CCR1+ cells.
Colorectal cancer
Prognosis
The expression of CCR1 is higher in colorectal
carcinoma than normal tissues, and correlates with
lymph node metastasis, deep invasion, poor
differentiation and advanced Dukes' stage.
Oncogenesis
Inactivation of TGF-beta family signaling within colon
cancer increases CCL9 and promotes recruitment of the
matrix metalloproteinase-expressing stromal cells that
carry CCR1. Lack of CCR1 prevents the accumulation
of MMP-expressing cells at the invasive front and
suppresses tumor invasion. In a murine model of
invasive colorectal cancer in which TGF-beta family
signaling is blocked, CD34+ CCR1+ immature myeloid
cell is recruited from the bone marrow to the tumor
invasive front where expression of CCL9 is increased.
These immature myeloid cells express MMP9, MMP2
and CCR1 and migrate toward the ligand CCL9. Lack
of CCR1 prevents accumulation of CD34+ immature
myeloid cell at the invasive front and suppresses tumor
invasion.
Prostate cancer
Oncogenesis
Androgen receptor negative human prostate cancer cell
line DU-145 cells selectively expressed CXCR4 and
CCR1 at high levels compared with DU-145/AR cells
that express androgen receptor. DU-145 showed
vigorous migratory responses to CXCL12 and CCL3.
In contrast, neither CXCL12 nor CCL3 affected the
migration of DU-145/AR cells.
Breast cancer
Oncogenesis
The expression of CCR5 was higher than that of CCR1
in the peripheral blood mononuclear cells (PBMC) of
healthy women, while the PBMC of the breast cancer
patients showed overexpression of CCR1 and
downregulation of CCR5. The differential effects of
MIP-1alpha and MIP-1beta on the PBMC of healthy
women and breast cancer patients correlated with the
expression levels of CCR1 and CCR5 in these
monocytes. In murine model of breast cancer, CCL5
(RANTES) was produced by the tumor cells, and its
receptors, CCR1 and CCR5, were expressed by the
infiltrating leukocytes. In mice treatment with MetCCL5, an antagonist of CCR1 and CCR5, the volume
and weight of tumors were significantly decreased
compared with control-treated tumors.
The total cell number obtained after collagenase
Non-small cell lung cancer
Oncogenesis
CCR1 expression correlated with the aggressive
phenotype of the non-small cell lung cancer (NSCLC)
cells. CCR1 knockdown significantly suppressed the
invasiveness of NSCLC cells and significantly reduced
the expression of matrix metalloproteinase-9, but had
only a minor effect on cell proliferation.
Atlas Genet Cytogenet Oncol Haematol. 2011; 15(1)
4
CCR1 (chemokine (C-C motif) receptor 1)
Gao Q, Fan J
Robinson SC, Scott KA, Wilson JL, Thompson RG, Proudfoot
AE, Balkwill FR. A chemokine receptor antagonist inhibits
experimental breast tumor growth. Cancer Res. 2003 Dec
1;63(23):8360-5
digestion was decreased in Met-CCL5-treated tumors
as was the proportion of infiltrating macrophages.
Furthermore, chemokine antagonist treatment increased
stromal development and necrosis.
Hurt EM, Wiestner A, Rosenwald A, Shaffer AL, Campo E,
Grogan T, Bergsagel PL, Kuehl WM, Staudt LM.
Overexpression of c-maf is a frequent oncogenic event in
multiple myeloma that promotes proliferation and pathological
interactions with bone marrow stroma. Cancer Cell. 2004
Feb;5(2):191-9
Glioma
Oncogenesis
Co-cultured human glioma U87 cells induced an
activated phenotype in HUVECs. These tumouractivated endothelial cells coordinately expressed
matching pairs of receptors/ligands were found to be,
including CCR1-RANTES axis.
Ko J, Jang SW, Kim YS, Kim IS, Sung HJ, Kim HH, Park JY,
Lee YH, Kim J, Na DS. Human LZIP binds to CCR1 and
differentially affects the chemotactic activities of CCR1dependent chemokines. FASEB J. 2004 May;18(7):890-2
Osteogenic sarcoma
Trentin L, Cabrelle A, Facco M, Carollo D, Miorin M, Tosoni A,
Pizzo P, Binotto G, Nicolardi L, Zambello R, Adami F, Agostini
C, Semenzato G. Homeostatic chemokines drive migration of
malignant B cells in patients with non-Hodgkin lymphomas.
Blood. 2004 Jul 15;104(2):502-8
Oncogenesis
The activities of phospholipase C (PLC), protein kinase
C delta (PKCdelta) and NF-kappaB were enhanced by
Lkn-1 (CCL15) stimulation on CCR1+ human
osteogenic sarcoma cells. Inhibitors of G protein, PLC,
PKCdelta and NF-kappaB inhibited the chemotactic
activity of Lkn-1 on CCR1+ osteogenic sarcoma cells
indicating that Lkn-1-induced chemotaxis involving
these signaling pathways.
Oba Y, Lee JW, Ehrlich LA, Chung HY, Jelinek DF, Callander
NS, Horuk R, Choi SJ, Roodman GD. MIP-1alpha utilizes both
CCR1 and CCR5 to induce osteoclast formation and increase
adhesion of myeloma cells to marrow stromal cells. Exp
Hematol. 2005 Mar;33(3):272-8
Ribeiro S, Horuk R. The clinical potential of chemokine
receptor antagonists. Pharmacol Ther. 2005 Jul;107(1):44-58
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This article should be referenced as such:
Iida N, Nakamoto Y, Baba T, Kakinoki K, Li YY, Wu Y,
Matsushima K, Kaneko S, Mukaida N. Tumor cell apoptosis
induces tumor-specific immunity in a CC chemokine receptor
Atlas Genet Cytogenet Oncol Haematol. 2011; 15(1)
Gao Q, Fan J. CCR1 (chemokine (C-C motif) receptor 1). Atlas
Genet Cytogenet Oncol Haematol. 2011; 15(1):1-6.
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