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Functional Correlation Between ROS and Cancer Stem Cells in Cancer Progression

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Handbook of Oxidative Stress in Cancer: Therapeutic Aspects

Abstract

Reactive oxygen species (ROS) are extremely active molecules which are primarily consequential to aerobic metabolism. They serve as a “double-edged sword” by playing a regulatory role in both promotion and suppression of tumor. Cancer cells maintain a state of high ROS levels, whereas cancer stem cells (CSCs) survive in low ROS level which is crucial to maintain the self-renewal and stemness. Tumor hypoxia in CSCs is known for its significant role in EMT which may lead to cancer progression. Surprisingly, the generation of cells having stem cell properties is possible through EMT signaling. Interdependence of hypoxia, ROS production, EMT, and CSCs has been posited in the retrospective literature. CSCs are characterized by unique properties such as resistance to radio- and chemotherapy when compared to non-CSCs. The observation of CSCs holding enhanced protection mechanism from ROS-induced stress and a different metabolism from the differentiated part of the tumor has opened up a novel avenue in research, and it started developing drugs targeting CSC-specific signaling. Hence, the strategies that could increase the ROS and oxidative stress in CSCs might assist in eradication of these parent cells and a comprehensive picture about the CSC niche, and decoding the mechanisms of redox regulation in CSCs could lead to the discovery of therapeutic approaches for cancer. The chapter summarizes the role of ROS-induced tumor angiogenesis, metastasis and inflammation, ROS in the maintenance of CSCs, CSCs in EMT, and therapeutic targeting of CSCs.

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Correspondence to V. Vijaya Padma .

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© 2022 Springer Nature Singapore Pte Ltd.

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Vishnupriya, P., Aparna, A., Vijaya Padma, V. (2022). Functional Correlation Between ROS and Cancer Stem Cells in Cancer Progression. In: Chakraborti, S. (eds) Handbook of Oxidative Stress in Cancer: Therapeutic Aspects. Springer, Singapore. https://doi.org/10.1007/978-981-16-5422-0_89

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