Diabetes and cancer incidence have risen tremendously over the years. Additionally, both cancer and diabetes share numerous risks, such as overweight, inactive lifestyles, older age, and smoking. Numerous methods have been suggested to connect obesity and diabetes to cancer advancements, such as increasing insulin/ Insulin-like growth factor I (IGF-1) signaling, lipid and glucose uptake and metabolism, shifts in the cytokine, chemokine, and adipokine profile also variations in the adipose tissue immediately adjacent to cancer spots. Diabetes has been found to have a complicated cancer-causing mechanism involving excessive reactive oxygen species (ROS) production, loss of critical macromolecules, chronic inflammation, and delayed repair, all of which contribute to carcinogenesis. Diabetes-associated epithelial-to-mesenchymal transition and endothelial-to-mesenchymal transition lead to the formation of cancer-associated fibroblasts in tumors by enabling tumor cells to extravasate via the endothelium and epithelium. This study aims to describe the correlation between diabetes and cancer, as well as summarize the molecular connections and shared pathways such as sex hormones, hyperglycemia, inflammation, insulin axis, metabolic symbiosis, and endoplasmic reticulum (ER) stress that exist between them.
Keywords: Biologic pathway; Cancer; Diabetes; Insulin; Malignancy.
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