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Oxidative stress arises from the inadequate production of reactive oxygen species (ROS) which couldn’t be neutralized by antioxidant defense. Cells maintain this balance of oxidants and antioxidants by different biochemical, metabolic and genetic mechanisms and in case of imbalance, several pathophysiological consequences can occur [1]. The crosstalk between cancer and oxidative stress is contradictory, either promoting tumorigenesis and cancer cell proliferation or stimulating apoptosis. The proliferation of cancer cells is accompanied by ROS overproduction; however, tumor cells balance this ROS threshold via an array of antioxidant systems to avoid ferroptosis, apoptosis or senescence [2]. On one hand, ROS scavenging by antioxidants could increase apoptosis and thus, deprives cancer cells of energy in early tumorigenesis. On the other hand, ROS production could selectively kill tumor cells by apoptosis, autophagy, necrosis and ferroptosis [3]. Therefore, the fine tuning between the ROS production and clearance is highly crucial. Among the key antioxidant systems, glutathione and thioredoxin pathways and Nrf2/Keap1 signaling systems have been reviewed in cancer [3]. In this context, peroxidation of the polyunsaturated fatty acids in the lipid bilayer of the cell membranes also gives rise to 4-hydroxynonenal (4-HNE), also known as the second messenger of ROS, which has been shown to exhibit a crucial role in cancer [4]. 4-HNE reportedly promotes cell proliferation, however, in some conditions it can stimulate apoptosis or necrosis of specific cancer cells [5]. 4-HNE exerts its effects by either binding to the arginine, histidine and …