Metformin (MET) is a preferred drug for the treatment of type 2 diabetes mellitus. Recent studies show that apart from its blood glucose-lowering effects, it also inhibits the development of various tumours, by inducing autophagy. Various studies have confirmed the inhibitory effects of MET on cancer cell lines’ propagation, migration, and invasion. The objective of the study was to comprehensively review the potential of MET as an anticancer agent, particularly focusing on its ability to induce autophagy and inhibit the development and progression of various tumors. The study aimed to explore the inhibitory effects of MET on cancer cell proliferation, migration, and invasion, and its impact on key signaling pathways such as AMPK, mTOR, and PI3K. This review noted that MET exerts its anticancer effects by regulating key signalling pathways such as phosphoinositide 3-kinase (PI3K), LC3-I and LC3-II, Beclin-1, p53, and the autophagy-related gene (ATG), inhibiting the mTOR protein, downregulating the expression of p62/SQSTM1, and blockage of the cell cycle at the G0/G1. Moreover, MET can stimulate autophagy through pathways associated with the 5′ adenosine monophosphate-activated protein kinase (AMPK), thereby inhibiting he development and progression of various human cancers, including hepatocellular carcinoma, prostate cancer, pancreatic cancer, osteosarcoma, myeloma, and non-small cell lung cancer. In summary, this detailed review provides a framework for further investigations that may appraise the autophagy-induced anticancer potential of MET and its repurposing for cancer treatment.

Diabetes mellitus (DM), a chronic metabolic disorder associated with hyperglycemia and other complications, is one of the five priority non communicable diseases of global interest with unprecedented rise in developing countries. Whereas, the current treatment with insulin and oral hypoglycemic agents is aimed at managing the hyperglycemia and associated complications, there is need to explore other critical pathways in the pathogenesis of DM that can act as potential drug targets with better treatment outcomes. This study comprehensively explains the role of cellular and molecular elements, like hyperglycemia-induced oxidative stress, endothelial dysfunction, and Nuclear Factor Kappa B (NF-κB)’s involvement in inflammation and immune regulation, in the onset of DM. With bioactive compounds from natural products gaining popularity as novel drug molecules due to their diverse pharmacological actions, the study also extensively explores the prospective therapeutic benefits of curcumin (CUR), a bioactive compound known for its antioxidant, anti-inflammatory, and hypoglycemic properties, in addressing diabetic complications, predominantly via the modulation of the NF-κB pathway. The findings reveal that CUR administration effectively lowered blood glucose elevation, reinstated diminished serum insulin levels, and enhanced body weight in Streptozotocin -induced diabetic rats. CUR exerts its beneficial effects in management of diabetic complications through regulation of signaling pathways, such as CaMKII, PPAR-γ, NF-κB, and TGF-β1. Moreover, CUR reversed the heightened expression of inflammatory cytokines (TNF-α, IL-1β, IL-6) and chemokines like MCP-1 in diabetic specimens, vindicating its anti-inflammatory potency in counteracting hyperglycemia-induced alterations. CUR diminishes oxidative stress, avert structural kidney damage linked to diabetic nephropathy, and suppress NF-κB activity. Furthermore, CUR exhibited a protective effect against diabetic cardiomyopathy, lung injury, and diabetic gastroparesis. Conclusively, the study posits that CUR could potentially offer therapeutic benefits in relieving diabetic complications through its influence on the NF-κB pathway.