EMT and inflammation: inseparable actors of cancer progression.
EMT and inflammation: inseparable actors of cancer progression.
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DOI：
10.1002/1878-0261.12095
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发表时间：
2017-07
影响因子：
6.6
通讯作者：
Gilles C
中科院分区：
文献类型：
--
作者：
Suarez-Carmona M;Lesage J;Cataldo D;Gilles C
肿瘤可以被描述为永远不会愈合的伤口，并且被大量的炎症和免疫细胞浸润。肿瘤相关的慢性炎症是癌症的标志，促进进展到转移阶段，最近已经进行了广泛的审查。事实上，持续存在于肿瘤中的炎性细胞与肿瘤细胞建立了相互作用，这可能导致表型转变为肿瘤支持细胞。这在巨噬细胞中得到了特别好的描述，被称为肿瘤相关的“M2”极化。上皮细胞向间质细胞转化（EMT）是一种胚胎程序，它使细胞-细胞粘附复合物松动，并赋予细胞增强的迁移和侵袭特性，可在转移进展期间被癌细胞吸收。经历EMT的癌细胞更具侵袭性，表现出更高的侵袭性、干细胞样特征和抗凋亡性。EMT程序还可以刺激癌细胞产生促炎因子。相反，炎症是肿瘤中EMT的有效诱导物。因此，这两种现象可能相互支持，在转移的联盟。这是本次审查的重点，EMT程序和炎症的细胞和分子演员之间的相互联系进行了描述。我们还概括了将EMT/炎症轴与转移联系起来的数据。
Tumors can be depicted as wounds that never heal, and are infiltrated by a large array of inflammatory and immune cells. Tumor‐associated chronic inflammation is a hallmark of cancer that fosters progression to a metastatic stage, as has been extensively reviewed lately. Indeed, inflammatory cells persisting in the tumor establish a cross‐talk with tumor cells that may result in a phenotype switch into tumor‐supporting cells. This has been particularly well described for macrophages and is referred to as tumor‐associated ‘M2’ polarization. Epithelial‐to‐mesenchymal transition (EMT), the embryonic program that loosens cell–cell adherence complexes and endows cells with enhanced migratory and invasive properties, can be co‐opted by cancer cells during metastatic progression. Cancer cells that have undergone EMT are more aggressive, displaying increased invasiveness, stem‐like features, and resistance to apoptosis. EMT programs can also stimulate the production of proinflammatory factors by cancer cells. Conversely, inflammation is a potent inducer of EMT in tumors. Therefore, the two phenomena may sustain each other, in an alliance for metastasis. This is the focus of this review, where the interconnections between EMT programs and cellular and molecular actors of inflammation are described. We also recapitulate data linking the EMT/inflammation axis to metastasis.