期刊
CURRENT STEM CELL RESEARCH & THERAPY
卷 5, 期 1, 页码 74-80出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/157488810790442813
关键词
Reactive oxygen species; EMT; cancer
资金
- National Cancer Institute, NIH [5R01CA101870]
- Department of Defense [W81XWH-08-1-0196]
- University of Texas MD Anderson Cancer Center [1P20-CA010193-01]
- Puschelberg and Guido Foundation
- NATIONAL CANCER INSTITUTE [P20CA101936, R01CA101870] Funding Source: NIH RePORTER
Reactive oxygen species (ROS) are known to serve as a second messenger in the intracellular signal transduction pathway for a variety of cellular processes, including inflammation, cell cycle progression, apoptosis, aging and cancer. Recently, ROS have been found to be associated with tumor metastasis involving the processes of tumor cell migration, invasion and angiogenesis. Emerging evidence also suggests that Epithelial-Mesenchymal Transition (EMT), a process that is reminiscent of cancer stem cells, is an important step towards tumor invasion and metastasis, and intimately involved in de novo and acquired drug resistance. In the light of recent advances, we are summarizing the role of ROS in EMT by cataloging how its deregulation is involved in EMT and tumor aggressiveness. Further attempts have been made to summarize the role of several chemopreventive agents that could be useful for targeted inactivation of ROS, suggesting that many natural agents could be useful for the reversal of EMT, which would become a novel approach for the prevention of tumor progression and/or the treatment of human malignancies especially by killing EMT-type cells that share similar characteristics with cancer stem cells.
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