anti-cancer properties of myricetin against ht-29 colon cancer cells through regulation of ripk1/ripk3 signaling pathway

Background: myricetin (mcn), a dietary flavonoid, is present in walnuts, fruits, vegetables, tea, and berries and has been suggested as an anti-inflammatory, antiplatelet, antimicrobial, antioxidant, and antiviral drug. objectives: this study aimed to investigate whether the necroptosis pathway involves the toxic impacts of myricetin (mcn) on the colon adenoma-carcinoma ht-29 cells. methods: for 48 hours, ht-29 cells were exposed to 50mmcnor threemmnecrosatine-1 (nec-1), a necroptosis preventive. apoptosis, cell viability, and expression of necroptosis-related genes, including mixed lineage kinase domain-like protein (mlkl), receptorinteracting protein kinase-1 (ripk1), and receptor-interacting protein kinase-3 (ripk3), were evaluated. results: mcn caused a noticeable decline in the survival of ht-29 cells. in contrast to the slight change in the apoptosis index in ht-29 cells, mcn considerably increased the necrosis index. mcn could enhance the expression of mlkl, ripk1, and ripk3 in the ht-29 cells. the co-treatment of mcn with nec-1 resulted in a significant elevation in ht-29 cell survival. nec-1 could decrease the necrosis index and expression of necroptosis-related proteins in the mcn-exposed ht-29 cells. conclusions: these findings demonstrated that mcn effectively induced cell death in ht-29 cells by activating the necroptosis pathway.