The Vicious Cross-Talk between Tumor Cells with an EMT Phenotype and Cells of the Immune System

被引:85
作者
Romeo, Elisabetta [1 ]
Caserta, Carmelo Antonio [1 ]
Rumio, Cristiano [2 ]
Marcucci, Fabrizio [2 ]
机构
[1] Fdn Med Solidale, Via San Cosimo 8 Pellaro, I-89134 Reggio Di Calabria, Italy
[2] Univ Milan, Dept Pharmacol & Biomol Sci, Via Trentacoste 2, I-20134 Milan, Italy
关键词
EMT; immune exclusion; immune deviation; cross-talk; cytokines; chemokines; exosomes; EPITHELIAL-MESENCHYMAL TRANSITION; PANCREATIC-CANCER CELLS; TGF-BETA; STAT3; ACTIVATION; T-CELLS; PROMOTE PROGRESSION; COLORECTAL-CANCER; PD-L1; EXPRESSION; DOWN-REGULATION; FEEDBACK LOOP;
D O I
10.3390/cells8050460
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Carcinoma cells that undergo an epithelial-mesenchymal transition (EMT) and display a predominantly mesenchymal phenotype (hereafter EMT tumor cells) are associated with immune exclusion and immune deviation in the tumor microenvironment (TME). A large body of evidence has shown that EMT tumor cells and immune cells can reciprocally influence each other, with EMT cells promoting immune exclusion and deviation and immune cells promoting, under certain circumstances, the induction of EMT in tumor cells. This cross-talk between EMT tumor cells and immune cells can occur both between EMT tumor cells and cells of either the native or adaptive immune system. In this article, we review this evidence and the functional consequences of it. We also discuss some recent evidence showing that tumor cells and cells of the immune system respond to similar stimuli, activate the expression of partially overlapping gene sets, and acquire, at least in part, identical functionalities such as migration and invasion. The possible significance of these symmetrical changes in the cross-talk between EMT tumor cells and immune cells is addressed. Eventually, we also discuss possible therapeutic opportunities that may derive from disrupting this cross-talk.
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页数:20
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