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Cancer Stem Cells: Reactive Oxygen Species-Induced Drug Resistance in Cancer

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Handbook of Oxidative Stress in Cancer: Therapeutic Aspects

Abstract

At present, there are several advancements in the field of cancer treatment that promise to increase the lifespan of a cancer patient. However, cancer recurrence and drug resistance are the challenges still faced in the field of cancer treatment. The normal production of cellular reactive oxygen species (ROS) plays a pivotal role in maintaining the cell quiescence and metabolism of stem cells. Overproduction of ROS leads to cell proliferation, differentiation, and apoptosis in a dose-exposure manner. Cancer stem cells (CSCs) could self-renew and protect themselves from exposure to toxic chemicals and free radicals. ROS are induced by several signaling molecules, such as growth factors, Wnt, Notch, and Hedgehog pathways. Recent studies have also suggested that microRNAs (miRNAs) induce ROS production and activate various signaling cascades to induce cell proliferation in cancer cells. In addition, chemotherapy activates the overexpression of cancer miRNAs in tumor cells, which induces the epithelial to mesenchymal transition that leads to therapeutic resistance. In most of the malignant conditions, miRNAs enhance the expression of signaling pathways in CSCs and activate cell proliferation. In this review, we provide an update to ROS-mediated therapeutic resistance in the signaling pathways of CSCs.

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Author Contributions

P.R. and S.J. wrote the manuscript. D.G. and K.P. edited the manuscript. All authors contributed to the article and approved the submitted version.

Funding

This study was supported by Department of Science and Technology (DST) Science Engineering Research Board (SERB), Government of India grant number EEQ/2017/000567 to KP.

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Rajendran, P. et al. (2022). Cancer Stem Cells: Reactive Oxygen Species-Induced Drug Resistance in Cancer. In: Chakraborti, S. (eds) Handbook of Oxidative Stress in Cancer: Therapeutic Aspects. Springer, Singapore. https://doi.org/10.1007/978-981-16-1247-3_217-1

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  • DOI: https://doi.org/10.1007/978-981-16-1247-3_217-1

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