## 1 Introduction  
Reactive oxygen species (ROS) are continuously released in aerobic organisms during cell metabolic reactions. ROS are very crucial in receptor activation, signal transduction, and gene expression [1]. The excessive production and insufficient removal of ROS result in oxidative stress that works as a significant risk factor in the pathogenesis of various diseases, including diabetes and cancer [2]. Oxidative stress results in the damage of various biomolecules such as DNA and RNA. Thus, ROS plays a very important role in the commencement of cancer [3]. The low concentration of ROS can result in tumor cell proliferation, survival, and tumor progression via the initiation of cellular signaling pathways that may lead to metastasis. However, the high concentrations of ROS have been reported to initiate cellular signaling pathways that may mediate the tumor cell death, as well as the formation of cancer stem cells. The formation of cancer stem cells may contribute to the recurrence of cancer [4]. Inflammation has been known to be linked with protein denaturation, membrane alteration, increased vascular permeability, and pain. However, chronic inflammation has been emphasized in tumor progression. The enhanced production of ROS at the site of inflammation results in tissue injury and endothelial dysfunction, resulting in inflammatory disorders [5]. The microenvironment of the tumor cells is mostly organized by inflammatory cells and is a crucial part of the neoplastic strategy that promotes proliferation, survival, and migration. Most of the signaling molecules associated with innate immune such as chemokines, selectins, and their specific receptors for invasion, migration, and metastases, have been co-opted by tumor cells [6]. The advanced glycation end products (AGEs) are diverse and highly reactive heterogenous formed due to the condensation of proteins with reducing sugars [7; 8; 9; 10; 11; 12]. The excessive accumulation of AGEs designates the state of total metabolic burden, chronic hyperglycemia, oxidative stress, and inflammation [9]. AGEs interact with specific receptors or bind proteins and activate a series of signaling pathways that are involved in diabetes-related complications such as diabetic nephropathy, cataract, Alzheimer's, atherosclerosis, etc. [13]. Besides, the cross-linking of proteins induced by AGEs leads to the formation of detergent-insoluble and proteinase-resistant aggregates. The presence of these aggregation products has been reported to the formation of autoantibodies in plasma and tissues of diabetic patients [14]. Besides, the relationship between accumulation of AGEs and development of vascular complications [15] and increased inflammation has been well documented. Chronic inflammation is an important cause of the development of cancer [16]. The increased level of AGEs in tumor cells has suggested its possible role in cancer progression [17]. The increased production of ROS and damaging of cell membranes are particularly common due to AGEs accumulation and are highlighted in gene mutations. Gene mutations are often associated with malignant cell transformation [18]. Many compounds and molecules have been reported to inhibit the formation of AGEs [19]. Several studies have reported that the use of natural products rich in compounds with strong antioxidant potential can be beneficial in the inhibition of protein modifications and AGEs formation [2] and in the reduction and prevention of several diabetic vascular complications. Recent research reported that plant-derived products could provide a better strategy for the treatment and prevention of many diseases. Various anticancer drugs such as vincristine, vinblastine, and camptothecin have been derived from plants [20]. _Phyllanthus emblica_ Linn. (_P. emblica_) (family Euphoriaceae) is commonly called gooseberry, and its fruit has been especially used as a traditional medicinal ingredient and in food items for several health-promoting effects and to treat a wide range of diseases [21]. _Azadirachta indica_ (_A.