Author Login

Authors:  Duaa e Fathah¹, Yasir Hameed², Samina Ejaz^1*, 

1. Department of Biochemistry, Institute of Biochemistry, Biotechnology, and Bioinformatics, IBBB. The Islamia University of Bahawalpur.
2. Department of Biotechnology, Institute of Biochemistry, Biotechnology, and Bioinformatics, IBBB. The Islamia University of Bahawalpur.

DOI: 10.52338/jcbc.2024.4221

Abstract:

Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) are the known enzymes in the human body that are exclusively involved in the production of reactive oxygen species (ROS). The trans-membrane protein NADPH oxidase is known to contain seven isoforms, NOX1-5 and DUOX1-2, which catalyze the generation of reactive oxygen species (ROS) needed for a variety of cellular functions. Strong anti-oxidant networks are necessary for cells to scavenge ROS and shield biological components from oxidative damage because too much ROS causes oxidative stress. The overexpression of NOX isoforms is typically linked to the carcinogenesis of several types of carcinomas, including breast cancer (BC). Because NOX isoforms are overexpressed in BC, they cause oxidative stress, damage mtDNA, and promote angiogenesis and EMT, which in turn aid in BC spreading. With the exception of BC, a number of NOX inhibitors are being used to treat different diseases. Although numerous researchers have suggested that blocking NOX activity is a viable therapeutic approach for individuals with various types of cancer, the therapeutic utility of this approach has not yet been confirmed by clinical trials. Given that breast cancer is the most frequent cancer globally, it’s critical to comprehend how ROS and NOX isoforms contribute to the pathobiology of the disease and investigate the possible therapeutic applications of NOX inhibitors in the treatment of breast cancer. In an effort to validate the role of NOX inhibitors as a successful therapeutic approach to controlling BC, this review paper attempts to give a thorough explanation of the involvement of NOX isoforms in the promotion of metastasis associated with BC.

Citation:

Dr.Samina Ejaz. Oxidative Stress induced by Over-Expressed NADPH Oxidase (NOX) Initiates Breast Cancer, Promotes Metastasis via Epithelial to Mesenchymal Transition (EMT), Remodels Chromatin and Confers Drug Resistance. Journal of Clinical Breast Cancer 2024