Transforming growth factor-beta and matrix metalloproteinases: functional interactions in tumor stroma-infiltrating myeloid cells.
Transforming growth factor-beta and matrix metalloproteinases: functional interactions in tumor stroma-infiltrating myeloid cells.
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DOI：
10.1155/2014/521754
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发表时间：
2014-01-01
影响因子：
--
通讯作者：
Santibanez, Juan F
中科院分区：
文献类型：
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作者：
Krstic, Jelena;Santibanez, Juan F
转化生长因子-β（TGF-β）是一种多效性因子，在健康和疾病中具有几种不同的作用。在肿瘤发生中，它可能作为促肿瘤发生因子，并对免疫系统反应的调节产生深远影响。基质金属蛋白酶（Matrix metalloproteinases，MMPs）是一个由25个以上成员组成的家族，近年来被认为是肿瘤间质中重要的调节因子，通过调节非细胞和细胞微环境的反应而发挥作用。肿瘤间质由骨髓来源的多种类型的驻留细胞和浸润细胞组成，它们共同在促进肿瘤生长和转移中起关键作用。在癌细胞中，TGF-β调节MMP的表达，而由癌细胞或居民基质细胞产生的MMP激活细胞外基质中的潜伏TGF-β，共同促进肿瘤进展的增强。在这篇综述中，我们将重点放在髓样基质细胞，如肿瘤相关的巨噬细胞，中性粒细胞，树突状细胞和肥大细胞，这是有力的调节TGF-β和产生大量的MMP的隔室。他们的相互作用和相互影响的生成促肿瘤发生的癌症微环境将进行分析。
Transforming growth factor-beta (TGF-beta) is a pleiotropic factor with several different roles in health and disease. In tumorigenesis, it may act as a protumorigenic factor and have a profound impact on the regulation of the immune system response. Matrix metalloproteinases (MMPs) are a family that comprises more than 25 members, which have recently been proposed as important regulators acting in tumor stroma by regulating the response of noncellular and cellular microenvironment. Tumor stroma consists of several types of resident cells and infiltrating cells derived from bone marrow, which together play crucial roles in the promotion of tumor growth and metastasis. In cancer cells, TGF-beta regulates MMPs expression, while MMPs, produced by either cancer cells or residents' stroma cells, activate latent TGF-beta in the extracellular matrix, together facilitating the enhancement of tumor progression. In this review we will focus on the compartment of myeloid stroma cells, such as tumor-associated macrophages, neutrophils, and dendritic and mast cells, which are potently regulated by TGF-beta and produce large amounts of MMPs. Their interplay and mutual implications in the generation of pro-tumorigenic cancer microenvironment will be analyzed.