Myricetin is categorized under the secondary metabolite flavonoid which includes a diverse range of consumable plant parts, and it has a potential against several classes of cancer including cancers and tumors. In the present study, the anticancer potential of the unique flavonoid-myricetin in A549 lung cancer cells was evaluated. Among different doses of myricetin, 73 μg/ml was more effective to prevent the cancer cell growth. It also promoted sub-G1 phase aggregation of cells and a equivalent decrease in the fraction of cells entering the S and subsequent phase which indicates apoptotic cell death. Myricetin generated enormous free radicals and, altered the potential of mitochondrial membrane in A549 cells as paralleled to untreated cells. In addition, myricetin treatment intensified the expression of P53 and relegated the expression of EGFR in A549 cells. These results suggested that myricetin exhibits cytotoxic potential by arresting the progression of cell cycle and ROS-dependent mitochondria-mediated mortality in cancer A549 lung cancer cells and it would be useful to develop as a drug candidate for lung cancer therapeutics. In silico experiments were carried out against human EGFR and P53 tumor suppressor protein to gain more insights into the binding mode of the myricetin may act as significant potential for anticancer therapy.
Keywords: A549 cells; Apoptosis; EGFR; MMP; Molecular docking; Myricetin; P53 activation.