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J Clin Med. 2019 May 25;8(5). pii: E747. doi: 10.3390/jcm8050747.

Epithelial-Mesenchymal Plasticity in Organotropism Metastasis and Tumor Immune Escape.

Author information

1
Center for Biomedical Engineering, University of Science and Technology of China, Hefei 230052, China. xnan2@houstonmethodist.org.
2
Department of Systems Medicine and Bioengineering, Houston Methodist Cancer Center, Weill Cornell Medicine, Houston, TX 77030, USA. xnan2@houstonmethodist.org.
3
Department of Orthopedics, Tongji Hospital, Wuhan 430050, China. wangjiangtjgk@163.com.
4
Department of Systems Medicine and Bioengineering, Houston Methodist Cancer Center, Weill Cornell Medicine, Houston, TX 77030, USA. hnliu@houstonmethodist.org.
5
Department of Systems Medicine and Bioengineering, Houston Methodist Cancer Center, Weill Cornell Medicine, Houston, TX 77030, USA. stwong@houstonmethodist.org.
6
Department of Systems Medicine and Bioengineering, Houston Methodist Cancer Center, Weill Cornell Medicine, Houston, TX 77030, USA. hzhao@houstonmethodist.org.

Abstract

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.

KEYWORDS:

EMT heterogeneity; cell–cell communication; organotropism metastasis; tumor immune escape

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