Abstract
C-C motif ligand 2 (CCL2) was originally reported as a chemical mediator attracting mononuclear cells to inflammatory tissue. Many studies have reported that CCL2 can directly activate cancer cells through a variety of mechanisms. CCL2 can also promote cancer progression indirectly through increasing the recruitment of tumor-associated macrophages into the tumor microenvironment. The role of CCL2 in cancer progression has gradually been understood, and various preclinical cancer models elucidate that CCL2 and its receptor C-C chemokine receptor 2 (CCR2) are attractive targets for intervention in cancer development. However, clinically available drugs that regulate the CCL2–CCR2 axis as anticancer agents are not available at this time. The complete elucidation of not only the oncological but also the physiological functions of the CCL2–CCR2 axis is required for achieving a satisfactory effect of the CCL2–CCR2 axis-targeted therapy.
Highlights
C-C motif ligand 2 (CCL2) was discovered first among CC chemokines in 1989 and helped to propel subsequent discoveries of other CC chemokines [1]
Many studies have proven the key roles of the CCL2–chemokine receptor 2 (CCR2) axis in tumor progression in a variety of cancers, there are no clinically available drugs that can modulate the CCL2–CCR2 axis as anticancer agents so far
A high serum CCL2 level may reflect the activity of cancer cells because CCL2 is produced by them; some studies have reported conflicting results that a low serum CCL2 level contributed to a worse prognosis in cancer patients [109]
Summary
C-C motif ligand 2 (CCL2) was discovered first among CC chemokines in 1989 and helped to propel subsequent discoveries of other CC chemokines [1]. Studies on the role of CCL2 in cancer have been reported since 2000, and the role of CCL2 in the tumor microenvironment, immuno-oncology, and cancer cells has been the main topic of CCL2 research nowadays. Other chemokines, such as CCL18 and CCL20, have been reported to play important roles in the growth and migration of various cancers and have been shown to be promising as tumor markers and therapeutic targets, but have not yet reached clinical application [10,11]. The potentials and limitations of CCL2–CCR2 axis targeted as cancer immunotherapy and a diagnostic tool are described in this review
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