Epithelial-Mesenchymal Plasticity in Organotropism Metastasis and Tumor Immune Escape

被引：18

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

来源：

JOURNAL OF CLINICAL MEDICINE | 2019年 / 8卷 / 05期

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

页数：16

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