Interplay between Inflammation and Stemness in Cancer Cells: The Role of Toll-Like Receptor Signaling
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-) m...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2016/4368101 |
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| author | Da-Wei Yeh Li-Rung Huang Ya-Wen Chen Chi-Ying F. Huang Tsung-Hsien Chuang |
| author_facet | Da-Wei Yeh Li-Rung Huang Ya-Wen Chen Chi-Ying F. Huang Tsung-Hsien Chuang |
| author_sort | Da-Wei Yeh |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-0dd26966599b48ad9810b950eee570a0 |
| institution | Kabale University |
| issn | 2314-8861 2314-7156 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Immunology Research |
| spelling | doaj-art-0dd26966599b48ad9810b950eee570a02025-02-03T00:59:03ZengWileyJournal of Immunology Research2314-88612314-71562016-01-01201610.1155/2016/43681014368101Interplay between Inflammation and Stemness in Cancer Cells: The Role of Toll-Like Receptor SignalingDa-Wei Yeh0Li-Rung Huang1Ya-Wen Chen2Chi-Ying F. Huang3Tsung-Hsien Chuang4Immunology Research Center, National Health Research Institutes, Miaoli 35053, TaiwanInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli 35053, TaiwanNational Institute of Cancer Research, National Health Research Institutes, Miaoli 35053, TaiwanInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei 11221, TaiwanImmunology Research Center, National Health Research Institutes, Miaoli 35053, TaiwanCancer 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.http://dx.doi.org/10.1155/2016/4368101 |
| spellingShingle | Da-Wei Yeh Li-Rung Huang Ya-Wen Chen Chi-Ying F. Huang Tsung-Hsien Chuang Interplay between Inflammation and Stemness in Cancer Cells: The Role of Toll-Like Receptor Signaling Journal of Immunology Research |
| title | Interplay between Inflammation and Stemness in Cancer Cells: The Role of Toll-Like Receptor Signaling |
| title_full | Interplay between Inflammation and Stemness in Cancer Cells: The Role of Toll-Like Receptor Signaling |
| title_fullStr | Interplay between Inflammation and Stemness in Cancer Cells: The Role of Toll-Like Receptor Signaling |
| title_full_unstemmed | Interplay between Inflammation and Stemness in Cancer Cells: The Role of Toll-Like Receptor Signaling |
| title_short | Interplay between Inflammation and Stemness in Cancer Cells: The Role of Toll-Like Receptor Signaling |
| title_sort | interplay between inflammation and stemness in cancer cells the role of toll like receptor signaling |
| url | http://dx.doi.org/10.1155/2016/4368101 |
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