Epithelial-mesenchymal plasticity in organotropism metastasis and tumor immune escape

Xiang Nan; Jiang Wang; Haowen Nikola Liu; Stephen T.C. Wong; Hong Zhao

doi:10.3390/jcm8050747

Epithelial-mesenchymal plasticity in organotropism metastasis and tumor immune escape

Xiang Nan, Jiang Wang, Haowen Nikola Liu, Stephen T.C. Wong, Hong Zhao

Research output: Contribution to journal › Review article › peer-review

14 Scopus citations

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.

Original language	English (US)
Article number	747
Journal	Journal of Clinical Medicine
Volume	8
Issue number	5
DOIs	https://doi.org/10.3390/jcm8050747
State	Published - May 2019

Keywords

Cell
Cell communication
EMT heterogeneity
Organotropism metastasis
Tumor immune escape

ASJC Scopus subject areas

Medicine(all)

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10.3390/jcm8050747

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title = "Epithelial-mesenchymal plasticity in organotropism metastasis and tumor immune escape",

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 = "Cell, Cell communication, EMT heterogeneity, Organotropism metastasis, Tumor immune escape",

author = "Xiang Nan and Jiang Wang and Liu, {Haowen Nikola} and Wong, {Stephen T.C.} and Hong Zhao",

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T1 - Epithelial-mesenchymal plasticity in organotropism metastasis and tumor immune escape

AU - Nan, Xiang

AU - Wang, Jiang

AU - Liu, Haowen Nikola

AU - Wong, Stephen T.C.

AU - Zhao, Hong

PY - 2019/5

Y1 - 2019/5

N2 - 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.

AB - 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.

KW - Cell

KW - Cell communication

KW - EMT heterogeneity

KW - Organotropism metastasis

KW - Tumor immune escape

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Epithelial-mesenchymal plasticity in organotropism metastasis and tumor immune escape

Abstract

Keywords

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