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Journal of Immunology Research
Volume 2016, Article ID 4368101, 14 pages
Review Article

Interplay between Inflammation and Stemness in Cancer Cells: The Role of Toll-Like Receptor Signaling

1Immunology Research Center, National Health Research Institutes, Miaoli 35053, Taiwan
2Institute of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli 35053, Taiwan
3National Institute of Cancer Research, National Health Research Institutes, Miaoli 35053, Taiwan
4Institute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei 11221, Taiwan
5Program in Environmental and Occupational Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan

Received 18 September 2016; Revised 22 November 2016; Accepted 5 December 2016

Academic Editor: Andréia M. Cardoso

Copyright © 2016 Da-Wei Yeh et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cancer stem cells (CSCs) are a small population of cancer cells that exhibit stemness. These cells contribute to cancer metastasis, treatment resistance, and relapse following therapy; therefore, they may cause malignancy and reduce the success of cancer treatment. Nuclear factor kappa B- (NF-κB-) mediated inflammatory responses increase stemness in cancer cells, and CSCs constitutively exhibit higher NF-κB activation, which in turn increases their stemness. These opposite effects form a positive feedback loop that further amplifies inflammation and stemness in cancer cells, thereby expanding CSC populations in the tumor. Toll-like receptors (TLRs) activate NF-κB-mediated inflammatory responses when stimulated by carcinogenic microbes and endogenous molecules released from cells killed during cancer treatment. NF-κB activation by extrinsic TLR ligands increases stemness in cancer cells. Moreover, it was recently shown that increased NF-κB activity and inflammatory responses in CSCs may be caused by altered TLR signaling during the enrichment of stemness in cancer cells. Thus, the activation of TLR signaling by extrinsic and intrinsic factors drives a positive interplay between inflammation and stemness in cancer cells.