Anti-cancer Properties of Myricetin Against HT-29 Colon Cancer Cells Through Regulation of RIPK1/RIPK3 Signaling Pathway
| Author | Hadis Alidadi | en |
| Author | Azin Samimi | en |
| Author | Masoud Ali Karami | en |
| Author | Layasadat Khorsandi | en |
| Author | Atefeh Ashtari | en |
| Orcid | Layasadat Khorsandi [0000-0002-3391-3055] | en |
| Issued Date | 2022-06-30 | en |
| Abstract | 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 50 µM MCN or three mM Necrosatine-1 (Nec-1), a necroptosis preventive. Apoptosis, cell viability, and expression of necroptosis-related genes, including mixed lineage kinase domain-like protein (MLKL), receptor-interacting 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. | en |
| DOI | https://doi.org/10.5812/jjcmb-129878 | en |
| Keyword | Myricetin | en |
| Keyword | Necroptosis | en |
| Keyword | Colon Cancer | en |
| Keyword | Cytotoxicity | en |
| Publisher | Brieflands | en |
| Title | Anti-cancer Properties of Myricetin Against HT-29 Colon Cancer Cells Through Regulation of RIPK1/RIPK3 Signaling Pathway | en |
| Type | Research Article | en |