Reactive oxygen species produced by altered tumor metabolism impacts cancer stem cell maintenance
Redox Biology, ISSN: 2213-2317, Vol: 44, Page: 101953
2021
- 52Citations
- 49Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations52
- Citation Indexes52
- 52
- CrossRef42
- Captures49
- Readers49
- 49
Article Description
Controlling reactive oxygen species (ROS) at sustainable levels can drive multiple facets of tumor biology, including within the cancer stem cell (CSC) population. Tight regulation of ROS is one key component in CSCs that drives disease recurrence, cell signaling, and therapeutic resistance. While ROS are well-appreciated to need oxygen and are a product of oxidative phosphorylation, there are also important roles for ROS under hypoxia. As hypoxia promotes and sustains major stemness pathways, further consideration of ROS impacts on CSCs in the tumor microenvironment is important. Furthermore, glycolytic shifts that occur in cancer and may be promoted by hypoxia are associated with multiple mechanisms to mitigate oxidative stress. This altered metabolism provides survival advantages that sustain malignant features, such as proliferation and self-renewal, while producing the necessary antioxidants that reduce damage from oxidative stress. Finally, disease recurrence is believed to be attributed to therapy resistant CSCs which can be quiescent and have changes in redox status. Effective DNA damage response pathways and/or a slow-cycling state can protect CSCs from the genomic catastrophe induced by irradiation and genotoxic agents. This review will explore the delicate, yet complex, relationship between ROS and its pleiotropic role in modulating the CSC.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2213231721001014; http://dx.doi.org/10.1016/j.redox.2021.101953; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85106652906&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/34052208; https://linkinghub.elsevier.com/retrieve/pii/S2213231721001014; https://dx.doi.org/10.1016/j.redox.2021.101953
Elsevier BV
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