巨噬细胞通过调节癌细胞中的泛素特异性肽酶17促进肺癌的进展

Chih-hao Lu, Chao-Yang Lai, T. Chuang
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引用次数: 0

摘要

收稿日期:2018年9月28日;录用日期:2018年10月12日;肿瘤相关巨噬细胞(tumor -associated macrophages, tam)是肿瘤微环境中的基质细胞,影响肿瘤的发展。巨噬细胞根据其功能可分为不同的亚群。一个简单的模型是,M1(或经典活化)巨噬细胞有利于恶性细胞的免疫监视,M2(或选择性活化)巨噬细胞发挥免疫抑制作用并发挥肿瘤功能。tam并不是一个统一的群体。它们表现出介于M1和M2巨噬细胞表型之间的特征。在某些类型的癌症中,如肺癌,tam的广泛积累往往与预后不良有关。除了调节免疫反应外,tam还通过调节癌细胞的增殖、侵袭和转移来促进肿瘤进展。因此,研究巨噬细胞与癌细胞相互作用构建原肿瘤微环境的分子机制,旨在制定抗肿瘤策略[1-4]。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Macrophages promote progression of lung cancer by regulating ubiquitin-specific peptidase 17 in cancer cells
Received: September 28, 2018; Accepted: October 12, 2018; Published: October 16, 2018 Tumor-associated macrophages (TAMs) are stromal cells in the tumor microenvironment that affect the progression of tumor development. Macrophages can be divided into different subsets based on their functions. A simplistic model is that M1 (or classically activated) macrophages favor the immunosurveillance of malignant cells and M2 (or alternatively activated) macrophages exert immunosuppressive effects and perform protumoral functions. TAMs are not a single uniform population. They exhibit features that are intermediate between the M1 and M2 macrophage phenotypes. In some cancer types such as lung cancer, extensive accumulation of TAMs is often associated with poor prognosis. In addition to the regulation of immunological responses, TAMs promote tumor progression through the regulation of cancer cell proliferation, invasion, and metastasis. Therefore, the molecular mechanisms underlying the interaction between macrophages and cancer cells to build a protumoral microenvironment were investigated with the goal of developing antitumor strategies [1-4].
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