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• W4285183296 abstract "Cancer is one of the major causes of death worldwide, and persistent oxidative stress is considered as a proactive contributor to its pathogenesis. Oxidative stress is mainly identified by an increased level of reactive oxygen species (ROS) and reduced antioxidant defense system. Various exogenous and endogenous factors and altered metabolic processes produce different types of ROS that cause DNA damage, mutation, production of pro-carcinogens, and induced programmed cell death. These ROS alter various signaling pathways such as NF-kB, Nrf2, Akt/PI3K/mTOR, MAPK, p53, etc. which further regulate other downstream signaling molecules such as CREB, c-Myc, c-Jun, c-fos, etc., leading to initiation and progression of tumorigenesis. ROS also regulate the mechanism of angiogenesis and ensure the growth, survival, as well as invasion of tumor cells. Apart from cross talk between different signaling molecules, ROS and miRNAs work in close proximity and participate in tumorigenesis. Looking into the pro-carcinogenic role of ROS, many natural and synthetic antioxidants have been explored for their anticancer effect. These antioxidants not only abrogate the progression, proliferation, and invasion of tumors but also protect the healthy cells from the deleterious effect of anticancer drugs. However, another hypothesis justifies the anticancer effect of ROS and its need to increase the sensitivity of tumor cells toward the anticancer drug. Thus, it can be said that ROS act as a double-edged sword, and a fine line or boundary exists between the use of antioxidant drug and the need of ROS for management and treatment of cancer." @default.
• W4285183296 created "2022-07-14" @default.
• W4285183296 creator A5045432062 @default.
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• W4285183296 date "2022-01-01" @default.
• W4285183296 modified "2023-09-26" @default.
• W4285183296 title "Molecular Mechanism of Oxidative Stress in Cancer and Its Therapeutics" @default.
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• W4285183296 doi "https://doi.org/10.1007/978-981-16-1247-3_150-1" @default.
• W4285183296 hasPublicationYear "2022" @default.
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