Department of Hematology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Cell Commun Signal. 2024 Mar 12;22(1):177. doi: 10.1186/s12964-024-01544-7.
The incidence of multiple myeloma (MM), a type of blood cancer affecting monoclonal plasma cells, is rising. Although new drugs and therapies have improved patient outcomes, MM remains incurable. Recent studies have highlighted the crucial role of the chemokine network in MM's pathological mechanism. Gaining a better understanding of this network and creating an overview of chemokines in MM could aid in identifying potential biomarkers and developing new therapeutic strategies and targets.
To summarize the complicated role of chemokines in MM, discuss their potential as biomarkers, and introduce several treatments based on chemokines.
Pubmed, Web of Science, ICTRP, and Clinical Trials were searched for articles and research related to chemokines. Publications published within the last 5 years are selected.
Malignant cells can utilize chemokines, including CCL2, CCL3, CCL5, CXCL7, CXCL8, CXCL12, and CXCL13 to evade apoptosis triggered by immune cells or medication, escape from bone marrow and escalate bone lesions. Other chemokines, including CXCL4, CCL19, and CXCL10, may aid in recruiting immune cells, increasing their cytotoxicity against cancer cells, and inducing apoptosis of malignant cells.
Utilizing anti-tumor chemokines or blocking pro-tumor chemokines may provide new therapeutic strategies for managing MM. Inspired by developed CXCR4 antagonists, including plerixafor, ulocuplumab, and motixafortide, more small molecular antagonists or antibodies for pro-tumor chemokine ligands and their receptors can be developed and used in clinical practice. Along with inhibiting pro-tumor chemokines, studies suggest combining chemokines with chimeric antigen receptor (CAR)-T therapy is promising and efficient.
多发性骨髓瘤（MM）是一种影响单克隆浆细胞的血液癌，其发病率正在上升。尽管新的药物和疗法改善了患者的预后，但 MM 仍然无法治愈。最近的研究强调了趋化因子网络在 MM 病理机制中的关键作用。更好地了解这个网络，并对 MM 中的趋化因子进行综述，可能有助于确定潜在的生物标志物，并开发新的治疗策略和靶点。
总结趋化因子在 MM 中的复杂作用，讨论它们作为生物标志物的潜力，并介绍几种基于趋化因子的治疗方法。
在 Pubmed、Web of Science、ICTRP 和 ClinicalTrials 上搜索与趋化因子相关的文章和研究。选择发表在过去 5 年内的出版物。
恶性细胞可以利用趋化因子，包括 CCL2、CCL3、CCL5、CXCL7、CXCL8、CXCL12 和 CXCL13，来逃避免疫细胞或药物触发的细胞凋亡，逃避骨髓并加剧骨病变。其他趋化因子，包括 CXCL4、CCL19 和 CXCL10，可能有助于招募免疫细胞，增加其对癌细胞的细胞毒性，并诱导恶性细胞凋亡。
利用抗肿瘤趋化因子或阻断促肿瘤趋化因子可能为 MM 的治疗提供新的策略。受已开发的 CXCR4 拮抗剂（如plerixafor、ulocuplumab 和 motixafortide）的启发，更多针对促肿瘤趋化因子配体及其受体的小分子拮抗剂或抗体可以被开发并应用于临床实践。除了抑制促肿瘤趋化因子外，研究表明将趋化因子与嵌合抗原受体（CAR）-T 疗法相结合具有很大的潜力和效率。
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