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Mechanistic and Therapeutic Crosstalk of Lipid Peroxidation in Oxidative Stress and Breast Cancer

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Handbook of Oxidative Stress in Cancer: Therapeutic Aspects

Abstract

Breast cancer is the most frequently diagnosed and leading cancer with the highest morbidity worldwide in women. In the past few decades, researchers have applied so many strategies for treating and preventing breast cancer. Here, we will discuss a different critical aspect of tumor hypoxia, which occurs due to an imbalance between cellular oxygen and its supply to the cells. We have subsequently proposed that hypoxia-inducible factor prolyl hydroxylase has a crucial role in lipid peroxidation-mediated protection in breast cancer cells. Reactive oxygen species have a vital role in influencing breast cancer microenvironment, angiogenesis, metastasis, and survival in a concentration-dependent manner. Reactive oxygen species promote cell growth at low concentrations by activating MAPK/ERK1/2, p38, JNK, PI3K/AKT, NF-κB, MMPs, and VEGF. Still, at high concentrations, reactive oxygen species triggered the process of cell apoptosis. This chapter describes the metabolic adaptation, epigenetics, and glycolytic shift of the breast cancer cells. The lipid peroxidation method of free radical generation and the effect of reactive oxygen species in angiogenesis and apoptosis are also discussed. The targeted therapies of hypoxia like hypoxia prodrugs, gene therapy, and modulation of prolyl hydroxylase are the future targets for breast cancer treatment.

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Singh, M., Kaithwas, G. (2022). Mechanistic and Therapeutic Crosstalk of Lipid Peroxidation in Oxidative Stress and Breast Cancer. In: Chakraborti, S. (eds) Handbook of Oxidative Stress in Cancer: Therapeutic Aspects. Springer, Singapore. https://doi.org/10.1007/978-981-16-5422-0_154

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