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

0Citations
Citations of this article
1Readers
Mendeley users who have this article in their library.
Get full text

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.

Cite

CITATION STYLE

APA

Rajendran, P., Jayaraman, S., Munuswamy-Ramanujam, G., Kumar, R. C. S., Ramachandran, B., Sambandam, Y., … Palaniyandi, K. (2022). Cancer Stem Cells: Reactive Oxygen Species-Induced Drug Resistance in Cancer. In Handbook of Oxidative Stress in Cancer: Therapeutic Aspects: Volume 1 (Vol. 1, pp. 2381–2402). Springer Singapore. https://doi.org/10.1007/978-981-16-5422-0_217

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free