CC Chemokine Ligand-2: A Promising Target for Overcoming Anticancer Drug Resistance

Simple Summary Drug resistance is an obstacle to cancer therapy, and the underlying mechanisms are still being explored. CC chemokine ligand-2 (CCL2) is one of the key proinflammatory chemokines that regulate the migration and infiltration of multiple inflammatory cells, such as monocytes and macrophages. CCL2 can be secreted by tumor cells and multiple cell types, mediating the formation of the tumor-promoting and immunosuppressive microenvironment to promote cancer development, progression, and anticancer drug resistance. Notably, CCL2 is also frequently overexpressed in drug-resistant cancer cells. Here, we review recent findings regarding the role of CCL2 in the development of resistance to multiple anticancer reagents. In addition, the possible mechanisms by which CCL2 participates in anticancer drug resistance are discussed, which may provide new therapeutic targets for reversing cancer resistance. CC chemokine ligand-2 (CCL2), a proinflammatory chemokine that mediates chemotaxis of multiple immune cells, plays a crucial role in the tumor microenvironment (TME) and promotes tumorigenesis and development. Recently, accumulating evidence has indicated that CCL2 contributes to the development of drug resistance to a broad spectrum of anticancer agents, including chemotherapy, hormone therapy, targeted therapy, and immunotherapy. It has been reported that CCL2 can reduce tumor sensitivity to drugs by inhibiting drug-induced apoptosis, antiangiogenesis, and antitumor immunity. In this review, we mainly focus on elucidating the relationship between CCL2 and resistance as well as the underlying mechanisms. A comprehensive understanding of the role and mechanism of CCL2 in anticancer drug resistance may provide new therapeutic targets for reversing cancer resistance.

Automated summary

CCL2, a proinflammatory chemokine, plays a crucial role in regulating the migration and infiltration of inflammatory cells and promoting tumorigenesis in the tumor microenvironment. Recent studies have shown its involvement in the development of resistance to various anticancer agents, and its mechanisms include inhibiting drug-induced apoptosis, antiangiogenesis, and antitumor immunity. Understanding the role and mechanisms of CCL2 in anticancer drug resistance may lead to new therapeutic targets for overcoming cancer resistance.