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Immunological Consequences of Epithelial-Mesenchymal Transition in Tumor Progression.

作者信息

Chockley Peter J, Keshamouni Venkateshwar G

机构信息

Graduate Program in Immunology, University of Michigan Medical Center, Ann Arbor, MI 48109; and.

Graduate Program in Immunology, University of Michigan Medical Center, Ann Arbor, MI 48109; and Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109

出版信息

J Immunol. 2016 Aug 1;197(3):691-8. doi: 10.4049/jimmunol.1600458.


DOI:10.4049/jimmunol.1600458
PMID:27431984
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4955875/
Abstract

Microenvironments that tumor cells encounter are different during the stages of cancer progression-primary tumor, metastasis, and at the metastatic site. This suggests potential differences in immune surveillance of primary tumor and metastasis. Epithelial-mesenchymal transition (EMT) is a key reversible process in which cancer cells transition into highly motile and invasive cells for dissemination. Only a tiny proportion successfully metastasize, supporting the notion of metastasis-specific immune surveillance. EMT involves extensive molecular reprogramming of cells conferring many clinically relevant features to cancer cells and affects tumor cell interactions within the tumor microenvironment. We review the impact of tumor immune infiltrates on tumor cell EMT and the consequences of EMT in shaping the immune microenvironment of tumors. The usefulness of EMT as a model to investigate metastasis-specific immune surveillance mechanisms are also explored. Finally, we discuss potential implications of EMT for tumor immunogenicity, as well as current immunotherapies and future strategies.

摘要

相似文献

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本文引用的文献

[1]
Epithelial-Mesenchymal Transition Is Associated with a Distinct Tumor Microenvironment Including Elevation of Inflammatory Signals and Multiple Immune Checkpoints in Lung Adenocarcinoma.

Clin Cancer Res. 2016-7-15

[2]
Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy.

Cancer Discov. 2016-1-19

[3]
Neutrophil Extracellular Traps Promote the Development and Progression of Liver Metastases after Surgical Stress.

Cancer Res. 2016-3-15

[4]
Complement Component 3 Is Regulated by TWIST1 and Mediates Epithelial-Mesenchymal Transition.

J Immunol. 2016-2-1

[5]
Patrolling monocytes control tumor metastasis to the lung.

Science. 2015-11-20

[6]
A Patient-Derived, Pan-Cancer EMT Signature Identifies Global Molecular Alterations and Immune Target Enrichment Following Epithelial-to-Mesenchymal Transition.

Clin Cancer Res. 2016-2-1

[7]
Regulation of complement-dependent cytotoxicity by TGF-β-induced epithelial-mesenchymal transition.

Oncogene. 2016-4-14

[8]
IL-17-producing γδ T cells and neutrophils conspire to promote breast cancer metastasis.

Nature. 2015-6-18

[9]
Immune cell promotion of metastasis.

Nat Rev Immunol. 2015-2

[10]
Metastasis is regulated via microRNA-200/ZEB1 axis control of tumour cell PD-L1 expression and intratumoral immunosuppression.

Nat Commun. 2014-10-28

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