CC Chemokine Ligand-2: A Promising Target for Overcoming Anticancer Drug Resistance
Zhenbo Shi1,2, Jian Tu1,2, Ying Ying2,3
1The Clinical Trial Research Center, The First Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Abstract:
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.
Insights
CC chemokine ligand-2 (CCL2) promotes cancer development and drug resistance by affecting tumor microenvironment immunity and apoptosis. Understanding CCL2
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- CC chemokine ligand-2 (CCL2) is a key mediator of immune cell trafficking within the tumor microenvironment (TME).
- CCL2 is increasingly recognized for its role in promoting tumor growth and progression.
- Emerging evidence links CCL2 to resistance against various anticancer therapies.
Purpose of the Study:
- To review the multifaceted role of CCL2 in the development of anticancer drug resistance.
- To elucidate the underlying molecular mechanisms by which CCL2 confers resistance.
- To highlight CCL2 as a potential therapeutic target for overcoming cancer drug resistance.
Main Methods:
- Literature review focusing on studies investigating CCL2 and drug resistance.
- Analysis of preclinical and clinical data on CCL2's impact on treatment efficacy.
- Synthesis of mechanistic insights into CCL2-mediated resistance pathways.
Main Results:
- CCL2 contributes to resistance against chemotherapy, hormone therapy, targeted therapy, and immunotherapy.
- Mechanisms include inhibition of drug-induced apoptosis, suppression of antiangiogenesis, and modulation of antitumor immunity.
- CCL2's influence on the TME is central to its role in promoting drug resistance.
Conclusions:
- CCL2 is a significant factor in the development of resistance to diverse anticancer treatments.
- Targeting CCL2 may offer a viable strategy to re-sensitize tumors to therapy.
- Further research into CCL2 pathways is crucial for developing novel combination therapies.
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