Epithelial-Mesenchymal Plasticity in Organotropism Metastasis and Tumor Immune Escape

被引:17
|
作者
Nan, Xiang [1 ,2 ]
Wang, Jiang [3 ]
Liu, Haowen Nikola [2 ]
Wong, Stephen Tc [2 ]
Zhao, Hong [2 ]
机构
[1] Univ Sci & Technol China, Ctr Biomed Engn, Hefei 230052, Anhui, Peoples R China
[2] Weill Cornell Med, Dept Syst Med & Bioengn, Houston Methodist Canc Ctr, Houston, TX 77030 USA
[3] Tongji Hosp, Dept Orthoped, Wuhan 430050, Hubei, Peoples R China
关键词
organotropism metastasis; EMT heterogeneity; tumor immune escape; cell-cell communication; BREAST-CANCER METASTASIS; STEM-CELLS; BRAIN METASTASIS; LUNG METASTASIS; EMT; TRANSITION; GENES; ACTIVATION; MECHANISMS; COLONIZATION;
D O I
10.3390/jcm8050747
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Most cancer deaths are due to metastasis, and almost all cancers have their preferential metastatic organs, known as organotropism metastasis. Epithelial-mesenchymal plasticity has been described as heterogeneous and dynamic cellular differentiation states, supported by emerging experimental evidence from both molecular and morphological levels. Many molecular factors regulating epithelial-mesenchymal plasticity have tissue-specific and non-redundant properties. Reciprocally, cellular epithelial-mesenchymal plasticity contributes to shaping organ-specific pre-metastatic niche (PMN) including distinct local immune landscapes, mainly through secreted bioactive molecular factors. Here, we summarize recent progress on the involvement of tumor epithelial-mesenchymal plasticity in driving organotropic metastasis and regulating the function of different immune cells in organ-specific metastasis.
引用
收藏
页数:16
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