Abstract
Curcumin is a plant polyphenol in turmeric root and a potent antioxidant. It binds to antioxidant response elements for gene regulation by nuclear factor erythroid 2-related factor 2, thereby suppressing reactive oxygen species (ROS) and exerting anti-inflammatory, anti-infective and other pharmacological effects. Of note, curcumin induces oxidative stress in tumors. It binds to several enzymes in tumors, such as carbonyl reductases, glutathione S-transferase P1 and nicotinamide adenine dinucleotide phosphate to induce mitochondrial damage, increase ROS production and ultimately induce tumor cell death. However, the instability and poor pharmacokinetic profile of curcumin in vivo limit its clinical application. Therefore, the effects of curcumin in vivo may be enhanced through its combination with drugs, derivative development and nanocarriers. In the present review, the mechanisms of curcumin that induce tumor cell death through oxidative stress are discussed. In addition, the methods used to enhance the antitumor activity of curcumin are described. Finally, the existing knowledge on the functions of curcumin in tumors, particularly in terms of oxidative stress, are summarized to facilitate future curcumin research.
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