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Tumor-associated macrophage-derived cytokines enhance cancer stem-like characteristics through epithelial–mesenchymal transition

Authors Chen Y, Tan W, Wang C

Received 23 March 2018

Accepted for publication 12 May 2018

Published 4 July 2018 Volume 2018:11 Pages 3817—3826

DOI https://doi.org/10.2147/OTT.S168317

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 2

Editor who approved publication: Dr Yao Dai


Yongxu Chen,1,2,* Wei Tan,1 Changjun Wang1,2,*

1Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangdong Geriatric Institute, Guangzhou, Guangdong Province, People’s Republic of China; 2School of Medicine, South China University of Technology, Guangzhou, Guangdong Province, People’s Republic of China

*All authors contributed equally to this work

Abstract: Cancer stem cells are a small population of cells with the potential for self-renewal and multi-directional differentiation and are an important source of cancer initiation, treatment resistance, and recurrence. Epithelial–mesenchymal transition (EMT) is a process in which epithelial cells lose their epithelial phenotype and convert to mesenchymal cells. Recent studies have shown that cancer cells undergoing EMT can become stem-like cells. Many kinds of tumors are associated with chronic inflammation, which plays a role in tumor progression. Among the various immune cells mediating chronic inflammation, macrophages account for ~30%–50% of the tumor mass. Macrophages are highly infiltrative in the tumor microenvironment and secrete a series of inflammatory factors and cytokines, such as transforming growth factor (TGF)-β, IL-6, IL-10, and tumor necrosis factor (TNF)-α, which promote EMT and enhance the stemness of cancer cells. This review summarizes and discusses recent research findings on some specific mechanisms of tumor-associated macrophage-derived cytokines in EMT and cancer stemness transition, which are emerging targets of cancer treatment.

Keywords: macrophage, cancer stem cell, tumor immunology, inflammatory cytokine, tumor microenvironment

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