Tumor-associated macrophage-derived cytokines enhance cancer stem-like characteristics through epithelial-mesenchymal transition.

Tumor-associated macrophage-derived cytokines enhance cancer stem-like characteristics through epithelial-mesenchymal transition.
复制标题

肿瘤相关巨噬细胞衍生的细胞因子通过上皮间质转化增强癌症干细胞样特征

DOI:
10.2147/ott.s168317
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发表时间:
2018
影响因子:
4
通讯作者:
Wang C
Wang C
中科院分区:
医学3区
文献类型:
--
作者:
Chen Y;Tan W;Wang C

文献摘要

被引文献

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癌症细胞是一小撮细胞,具有自我更新和多方向分化的潜力,是癌症起始,治疗耐药性和复发性的重要来源。慢性炎症在介导的慢性炎症的各种免疫力中起作用。 )-α,促进EMT并增强癌细胞的干性。这篇综述总结并讨论了有关EMT和癌症干性过渡中与肿瘤相关的巨噬细胞衍生细胞因子的一些特定机制的最新研究结果,这些机制是癌症治疗的新兴靶标。
Cancer stem cells are a small population of cells with the potential for self-renewal and multi-directional differentiation and are an important source of cancer initiation, treatment resistance, and recurrence. Epithelial–mesenchymal transition (EMT) is a process in which epithelial cells lose their epithelial phenotype and convert to mesenchymal cells. Recent studies have shown that cancer cells undergoing EMT can become stem-like cells. Many kinds of tumors are associated with chronic inflammation, which plays a role in tumor progression. Among the various immune cells mediating chronic inflammation, macrophages account for ~30%–50% of the tumor mass. Macrophages are highly infiltrative in the tumor microenvironment and secrete a series of inflammatory factors and cytokines, such as transforming growth factor (TGF)-β, IL-6, IL-10, and tumor necrosis factor (TNF)-α, which promote EMT and enhance the stemness of cancer cells. This review summarizes and discusses recent research findings on some specific mechanisms of tumor-associated macrophage-derived cytokines in EMT and cancer stemness transition, which are emerging targets of cancer treatment.