Nrf2 Modulation in Breast Cancer

• Published in: Biomedicines Vol. 10; no. 10; p. 2668
• Main Authors: Ghareghomi, Somayyeh, Habibi-Rezaei, Mehran, Arese, Marzia, Saso, Luciano, Moosavi-Movahedi, Ali Akbar
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 01.10.2022; MDPI
• Subjects: Angiogenesis; antioxidant pathway; Antioxidants; Apoptosis; Breast cancer; Cell death; Cell growth; Cell survival; DNA damage; Gene expression; Genes; Genomes; Intermediates; Keap1-Nrf2; Kinases; Metabolism; Metabolites; Mutation; Neurodegenerative diseases; Neuromodulation; Nrf2 inhibitors; NRF2 protein; Oxidative stress; Phosphorylation; Physiological aspects; Proteins; Radiation therapy; Reactive oxygen species; Review; Transcription factors; Tumorigenesis; Iran
• ISSN: 2227-9059; 2227-9059
• DOI: 10.3390/biomedicines10102668

Reactive oxygen species (ROS) are identified to control the expression and activity of various essential signaling intermediates involved in cellular proliferation, apoptosis, and differentiation. Indeed, ROS represents a double-edged sword in supporting cell survival and death. Many common pathological processes, including various cancer types and neurodegenerative diseases, are inflammation and oxidative stress triggers, or even initiate them. Keap1-Nrf2 is a master antioxidant pathway in cytoprotective mechanisms through Nrf2 target gene expression. Activation of the Nfr2 pathway benefits cells in the early stages and reduces the level of ROS. In contrast, hyperactivation of Keap1-Nrf2 creates a context that supports the survival of both healthy and cancerous cells, defending them against oxidative stress, chemotherapeutic drugs, and radiotherapy. Considering the dual role of Nrf2 in suppressing or expanding cancer cells, determining its inhibitory/stimulatory position and targeting can represent an impressive role in cancer treatment. This review focused on Nrf2 modulators and their roles in sensitizing breast cancer cells to chemo/radiotherapy agents.