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Quantifying Cancer Epithelial-Mesenchymal Plasticity and its Association with Stemness and Immune Response
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Epithelial-Mesenchymal Plasticity in Organotropism Metastasis and Tumor Immune Escape

1
Center for Biomedical Engineering, University of Science and Technology of China, Hefei 230052, China
2
Department of Systems Medicine and Bioengineering, Houston Methodist Cancer Center, Weill Cornell Medicine, Houston, TX 77030, USA
3
Department of Orthopedics, Tongji Hospital, Wuhan 430050, China
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
J. Clin. Med. 2019, 8(5), 747; https://doi.org/10.3390/jcm8050747
Received: 25 March 2019 / Revised: 21 May 2019 / Accepted: 22 May 2019 / Published: 25 May 2019
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. View Full-Text
Keywords: organotropism metastasis; EMT heterogeneity; tumor immune escape; cell–cell communication organotropism metastasis; EMT heterogeneity; tumor immune escape; cell–cell communication
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MDPI and ACS Style

Nan, X.; Wang, J.; Liu, H.N.; Wong, S.T.; Zhao, H. Epithelial-Mesenchymal Plasticity in Organotropism Metastasis and Tumor Immune Escape. J. Clin. Med. 2019, 8, 747.

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