MCP‑1 targeting: Shutting off an engine for tumor development (Review)

A large amount of research has proven that monocyte chemotactic protein-1 (MCP-1) is associated with different types of disease, including autoimmune, metabolic and cardiovascular diseases. In addition, several studies have found that MCP-1 is associated with tumor development. MCP-1 expression leve...

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Bibliographic Details
Published inOncology letters Vol. 23; no. 1; p. 1
Main Authors Wang, Liang, Lan, Jinxin, Tang, Jiaping, Luo, Na
Format Journal Article
LanguageEnglish
Published Athens Spandidos Publications 01.01.2022
Spandidos Publications UK Ltd
D.A. Spandidos
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Summary:A large amount of research has proven that monocyte chemotactic protein-1 (MCP-1) is associated with different types of disease, including autoimmune, metabolic and cardiovascular diseases. In addition, several studies have found that MCP-1 is associated with tumor development. MCP-1 expression level in the tumor microenvironment is associated with tumor development, including in tumor invasion and metastasis, angiogenesis, and immune cell infltration. However, the precise mechanism involved is currently being investigated. MCP-1 exerts its effects mainly via the MCP-1/C-C motif chemokine receptor 2 axis and leads to the activation of classical signaling pathways, such as PI3K/Akt/mTOR, ERK/GSK-3[beta]/Snail, c-Raf/MEK/ERK and MAPK in different cells. The specific mechanism is still under debate; however, target therapy utilizing MCP-1 as a neutralizing antibody has been found to have a detrimental effect on tumor development. The aim of the present review was to examine the effect of MCP-1 on tumor development from several aspects, including its structure, its involvement in signaling pathways, the participating cells, and the therapeutic agents targeting MCP-1. The improved understanding into the structure of MCP-1 and the mechanism of action may facilitate new and practical therapeutic agents to achieve maximum performance in the treatment of patients with cancer.
Bibliography:Contributed equally
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2021.13144