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由环氧合酶-2精心调控的肿瘤微环境炎症特征促进上皮-间质转化。

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

作者信息

Gómez-Valenzuela Fernán, Escobar Enrico, Pérez-Tomás Ricardo, Montecinos Viviana P

机构信息

Department of Hematology-Oncology, Pontificia Universidad Católica de Chile, Santiago, Chile.

Department of Oral Pathology and Medicine, Faculty of Dentistry, University of Chile, Santiago, Chile.

出版信息

Front Oncol. 2021 Jun 10;11:686792. doi: 10.3389/fonc.2021.686792. eCollection 2021.

DOI:10.3389/fonc.2021.686792
PMID:34178680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8222670/
Abstract

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.

摘要

肿瘤微环境（TME）是指细胞外基质与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而动态的相互联系。TME通过维持炎症状态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。尽管上皮-间质转化（EMT）是一个促进恶性上皮细胞出现侵袭性表型的相关转移起始事件，但其与TME炎症状态的关系仍知之甚少。先前的证据有力地表明，环氧合酶-2（COX-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信号通路有关。这篇综述文章总结了在TME背景下，COX-2过表达如何协调EMT过程并促进初始转移相关事件。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19e5/8222670/dfcd5b4646c1/fonc-11-686792-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19e5/8222670/77f2b8d67966/fonc-11-686792-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19e5/8222670/77f2b8d67966/fonc-11-686792-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19e5/8222670/baba7830125e/fonc-11-686792-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19e5/8222670/c4d358d6ecbe/fonc-11-686792-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19e5/8222670/dfcd5b4646c1/fonc-11-686792-g004.jpg

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