The Inflammatory Profile of the Tumor Microenvironment, Orchestrated by Cyclooxygenase-2, Promotes Epithelial-Mesenchymal Transition.

The Inflammatory Profile of the Tumor Microenvironment, Orchestrated by Cyclooxygenase-2, Promotes Epithelial-Mesenchymal Transition.
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DOI:
10.3389/fonc.2021.686792
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发表时间:
2021
影响因子:
4.7
通讯作者:
Montecinos VP
Montecinos VP
中科院分区:
医学3区
文献类型:
--
作者:
Gómez-Valenzuela F;Escobar E;Pérez-Tomás R;Montecinos VP

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肿瘤微环境(TME)对应于细胞外基质和恶性细胞及其周围由免疫细胞和间充质细胞组成的基质之间复杂且动态的相互连接。TME通过维持炎症特征的细胞因子进行持续的细胞通讯,这有利于肿瘤进展、血管生成、细胞侵袭和转移。虽然上皮-间质转化(EMT)代表了一个相关的转移启动事件,促进恶性上皮细胞的侵袭性表型,其与TME的炎症特征的关系知之甚少。先前的证据有力地表明,环氧合酶-2(考克斯-2)过表达,一种与慢性未解决炎症相关的促炎酶,与常见的EMT信号通路相关。这篇综述文章总结了考克斯-2的过度表达,在TME的背景下,编排EMT过程,并促进初始转移相关的事件。
The tumor microenvironment (TME) corresponds to a complex and dynamic interconnection between the extracellular matrix and malignant cells and their surrounding stroma composed of immune and mesenchymal cells. The TME has constant cellular communication through cytokines that sustain an inflammatory profile, which favors tumor progression, angiogenesis, cell invasion, and metastasis. Although the epithelial-mesenchymal transition (EMT) represents a relevant metastasis-initiating event that promotes an invasive phenotype in malignant epithelial cells, its relationship with the inflammatory profile of the TME is poorly understood. Previous evidence strongly suggests that cyclooxygenase-2 (COX-2) overexpression, a pro-inflammatory enzyme related to chronic unresolved inflammation, is associated with common EMT-signaling pathways. This review article summarizes how COX-2 overexpression, within the context of the TME, orchestrates the EMT process and promotes initial metastatic-related events.
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