Redox regulation of cell state and fate
Lee, BWL PRAMILA BABAN GHODE ONG SEK TONG, DERRICK
Lee, BWL
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Abstract
The failure in effective cancer treatment is thought to be attributed to a subpopulation of tumor cells with stem cell-like properties. These cancer stem cells (CSCs) are intimately linked to tumor initiation, heterogeneity, maintenance, recurrence and metastasis. Increasing evidence supports the view that a tight redox regulation is crucial for CSC proliferation, tumorigenicity, therapy resistance and metastasis in many cancer types. Since the distinct metabolic and epigenetic states of CSCs may influence ROS levels, and hence their malignancy, ROS modulating agents hold promise in their utility as anti-CSC agents that may improve the durability of current cancer treatments. This review will focus on (i) how ROS levels are regulated for CSCs to elicit their hallmark features; (ii) the link between ROS and metabolic plasticity of CSCs; and (iii) how ROS may interface with epigenetics that would enable CSCs to thrive in a stressful tumor microenvironment and survive therapeutic insults.
Keywords
Cancer stem cells, Epigenetics, Metabolism, Reactive oxygen species, Therapeutics, Carcinogenesis, Cell Lineage, Epigenesis, Genetic, Humans, Neoplastic Stem Cells, Oxidation-Reduction, Reactive Oxygen Species
Source Title
Redox Biology
Publisher
Elsevier BV
Series/Report No.
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Date
2019-07-01
DOI
10.1016/j.redox.2018.11.014
Type
Review