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Epithelial-Mesenchymal Plasticity in Organotropism Metastasis and Tumor Immune Escape
被引:15
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.
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页数:16
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