Reactive oxygen species : a volatile driver of field cancerization and metastasis
Field cancerization and metastasis are the leading causes for cancer recurrence and mortality in cancer patients. The formation of primary, secondary tumors or metastasis is greatly influenced by multifaceted tumor-stroma interactions, in which stromal components of the tumor microenvironment (TME)...
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| Format: | Journal Article |
| Language: | English |
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2019
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| Online Access: | https://hdl.handle.net/10356/90028 http://hdl.handle.net/10220/49363 |
| _version_ | 1811688603104837632 |
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| author | Liao, Zehuan Chua, Damien Tan, Nguan Soon |
| author2 | School of Biological Sciences |
| author_facet | School of Biological Sciences Liao, Zehuan Chua, Damien Tan, Nguan Soon |
| author_sort | Liao, Zehuan |
| collection | NTU |
| description | Field cancerization and metastasis are the leading causes for cancer recurrence and mortality in cancer patients. The formation of primary, secondary tumors or metastasis is greatly influenced by multifaceted tumor-stroma interactions, in which stromal components of the tumor microenvironment (TME) can affect the behavior of the cancer cells. Many studies have identified cytokines and growth factors as cell signaling molecules that aid cell to cell communication. However, the functional contribution of reactive oxygen species (ROS), a family of volatile chemicals, as communication molecules are less understood. Cancer cells and various tumor-associated stromal cells produce and secrete a copious amount of ROS into the TME. Intracellular ROS modulate cell signaling cascades that aid in the acquisition of several hallmarks of cancers. Extracellular ROS help to propagate, amplify, and effectively create a mutagenic and oncogenic field which facilitate the formation of multifoci tumors and act as a springboard for metastatic tumor cells. In this review, we summarize our current knowledge of ROS as atypical paracrine signaling molecules for field cancerization and metastasis. Field cancerization and metastasis are often discussed separately; we offer a model that placed these events with ROS as the focal instigating agent in a broader “seed-soil” hypothesis. |
| first_indexed | 2024-10-01T05:34:50Z |
| format | Journal Article |
| id | ntu-10356/90028 |
| institution | Nanyang Technological University |
| language | English |
| last_indexed | 2024-10-01T05:34:50Z |
| publishDate | 2019 |
| record_format | dspace |
| spelling | ntu-10356/900282020-11-01T05:21:07Z Reactive oxygen species : a volatile driver of field cancerization and metastasis Liao, Zehuan Chua, Damien Tan, Nguan Soon School of Biological Sciences Lee Kong Chian School of Medicine (LKCMedicine) Science::Biological sciences Reactive Oxygen Species Field Cancerization Field cancerization and metastasis are the leading causes for cancer recurrence and mortality in cancer patients. The formation of primary, secondary tumors or metastasis is greatly influenced by multifaceted tumor-stroma interactions, in which stromal components of the tumor microenvironment (TME) can affect the behavior of the cancer cells. Many studies have identified cytokines and growth factors as cell signaling molecules that aid cell to cell communication. However, the functional contribution of reactive oxygen species (ROS), a family of volatile chemicals, as communication molecules are less understood. Cancer cells and various tumor-associated stromal cells produce and secrete a copious amount of ROS into the TME. Intracellular ROS modulate cell signaling cascades that aid in the acquisition of several hallmarks of cancers. Extracellular ROS help to propagate, amplify, and effectively create a mutagenic and oncogenic field which facilitate the formation of multifoci tumors and act as a springboard for metastatic tumor cells. In this review, we summarize our current knowledge of ROS as atypical paracrine signaling molecules for field cancerization and metastasis. Field cancerization and metastasis are often discussed separately; we offer a model that placed these events with ROS as the focal instigating agent in a broader “seed-soil” hypothesis. MOE (Min. of Education, S’pore) Published version 2019-07-16T04:35:22Z 2019-12-06T17:39:04Z 2019-07-16T04:35:22Z 2019-12-06T17:39:04Z 2019 Journal Article Liao, Z., Chua, D., & Tan, N. S. (2019). Reactive oxygen species : a volatile driver of field cancerization and metastasis. Molecular Cancer, 18(1), 65-. doi:10.1186/s12943-019-0961-y https://hdl.handle.net/10356/90028 http://hdl.handle.net/10220/49363 10.1186/s12943-019-0961-y en Molecular Cancer © 2019 The Author(s). This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. 10 p. application/pdf |
| spellingShingle | Science::Biological sciences Reactive Oxygen Species Field Cancerization Liao, Zehuan Chua, Damien Tan, Nguan Soon Reactive oxygen species : a volatile driver of field cancerization and metastasis |
| title | Reactive oxygen species : a volatile driver of field cancerization and metastasis |
| title_full | Reactive oxygen species : a volatile driver of field cancerization and metastasis |
| title_fullStr | Reactive oxygen species : a volatile driver of field cancerization and metastasis |
| title_full_unstemmed | Reactive oxygen species : a volatile driver of field cancerization and metastasis |
| title_short | Reactive oxygen species : a volatile driver of field cancerization and metastasis |
| title_sort | reactive oxygen species a volatile driver of field cancerization and metastasis |
| topic | Science::Biological sciences Reactive Oxygen Species Field Cancerization |
| url | https://hdl.handle.net/10356/90028 http://hdl.handle.net/10220/49363 |
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