肿瘤相关巨噬细胞是肿瘤相关慢性炎症中的关键细胞,促进肿瘤生长、增殖、血管生成、侵袭、转移及化疗抵抗。巨噬细胞根据环境不同大致可极化为经典活化型巨噬细胞(M1型)及替代活化型巨噬细胞(M2型)。环氧酶2、核因子KB、T0ll样受体信号途径、缺氧、原癌基因MYC、Notch信号通路及细胞因子等参与肿瘤相关巨噬细胞发生M1-M2型别转化。巨噬细胞的表型及功能随着肿瘤进展的不同阶段而变化,针对巨噬细胞的抗肿瘤药物治疗,应取决于肿瘤所处的阶段。
Tumor-associated macrophages (TAMs) are key cells in tumor-associated chronic inflammation, and can promote tumor growth, proliferation, angiogenesis, invasion, metastasis and chemotherapy resistance. Under different circumstances, macrophages can be polarized into classically activated macrophages (M1) and alternatively activated macrophages (M2). Cyclooxygenase 2, nuclear factor- KB, Toll like receptor (TLR) signaling pathway, anoxia, the protooncogene MYC, Notch signaling pathway and cytokines are all involved in the transition of TAMs from M1 to M2 phenotype. The phenotype and function of TAMs vary with tumor progression, so antitumor drug therapies targeting macrophages should depend on the sta~e of tumors.