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The role of CXC chemokines and their receptors in the progression and treatment of tumors

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Abstract

Chemokines are a class of functional chemotactic peptides that contribute to a number of tumor-related processes. They are functionally defined as soluble factors that are able to control the directional migration of leukocytes, in particular, during infection and inflammation. It appears, however, that the biological effects mediated by chemokines are far more complex, and virtually all cells, including many tumor cell types, can express chemokines and chemokine receptors. A growing body of evidence indicates that they also contribute to a number of tumor-related processes, such as tumor cell growth, angiogenesis/angiostasis, local invasion, and mediate organ-specific metastases of cancer. The CXC chemokine class is a subfamily of a large family of chemokines. During the occurrence and development of tumor cells, this chemokine class is often accompanied by a series of molecular and biological changes. The CXC chemokine subfamily is closely related to the body’s immune response to tumors and biological behaviors of tumors. In this paper, CXC chemokines and their role in the progression and treatment of tumors will be reviewed.

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Abbreviations

GPCR:

G protein-coupled receptor

ECM:

Extracellular matrix

INF:

Interferon

HHV-8:

Human herpes virus 8

MGSA:

Melanocyte growth stimulatory activity

MMP:

Matrix metalloproteinase

SCID:

Severe combined immunodeficiency

TKRs:

Tyrosine kinase receptors

PKC:

Protein kinase C

NSCLC:

Non-small cell lung cancer

SCLC:

Small cell lung cancer

DRAC:

Duffy antigen receptor for chemokines

bFGF:

Basic fibroblast growth factor

VEGF:

Vascular endothelial growth factor

ENA-78:

Epithelial neutrophil-activating peptide 78

BRAK:

Breast and kidney-expressed chemokine

DCs:

Dendritic cells

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Acknowledgments

We thank Dr. Yu Wang for his critical reading of the manuscript.

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Zhu, Q., Han, X., Peng, J. et al. The role of CXC chemokines and their receptors in the progression and treatment of tumors. J Mol Hist 43, 699–713 (2012). https://doi.org/10.1007/s10735-012-9435-x

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