Inflammatory alterations of the extracellular matrix in the tumor microenvironment.
Inflammatory alterations of the extracellular matrix in the tumor microenvironment.
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DOI：
10.3390/cancers3033189
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发表时间：
2011-08-09
期刊：
影响因子：
5.2
通讯作者：
Itano N
中科院分区：
文献类型：
--
作者：
Iijima J;Konno K;Itano N
癌细胞和宿主基质细胞之间的复杂相互作用导致“肿瘤微环境”的形成，其中炎性改变涉及肿瘤相关成纤维细胞和炎性白细胞的浸润，其有助于获得恶性特征，例如增加的癌细胞增殖、侵袭性、转移、血管生成和避免适应性免疫。实体瘤的微环境不仅由细胞区室组成，而且由生物活性物质组成，包括细胞因子、生长因子和细胞外基质（ECM）。ECM可以作为细胞迁移的支架、细胞因子和生长因子的储存库以及通过受体结合的信号。在炎症过程中，ECM组分及其降解片段在某些情况下直接或间接地作为炎症刺激物，并调节炎症和免疫细胞的功能。一种这样的ECM组分，透明质酸，最近被认为通过模式识别toll样受体调节先天免疫细胞功能，并加速炎症癌症中肿瘤相关巨噬细胞的募集和激活。在这里，我们将总结肿瘤微环境中炎症与ECM重塑之间的分子机制，特别强调透明质酸在控制炎症反应中的作用。
Complex interactions between cancer cells and host stromal cells result in the formation of the “tumor microenvironment”, where inflammatory alterations involve the infiltration of tumor-associated fibroblasts and inflammatory leukocytes that contribute to the acquisition of malignant characteristics, such as increased cancer cell proliferation, invasiveness, metastasis, angiogenesis, and avoidance of adaptive immunity. The microenvironment of a solid tumor is comprised not only of cellular compartments, but also of bioactive substances, including cytokines, growth factors, and extracellular matrix (ECM). ECM can act as a scaffold for cell migration, a reservoir for cytokines and growth factors, and a signal through receptor binding. During inflammation, ECM components and their degraded fragments act directly and indirectly as inflammatory stimuli in certain cases and regulate the functions of inflammatory and immune cells. One such ECM component, hyaluronan, has recently been implicated to modulate innate immune cell function through pattern recognition toll-like receptors and accelerate the recruitment and activation of tumor-associated macrophages in inflamed cancers. Here, we will summarize the molecular mechanism linking inflammation with ECM remodeling in the tumor microenvironment, with a particular emphasis on the role of hyaluronan in controlling the inflammatory response.