The toxicological role of Myricetin in the progression of human anaplastic thyroid cancer SW1736 cell line.

AIMS AND BACKGROUND

Anaplastic thyroid cancer cells lack the capacity to effectively accumulate iodine and are therefore unresponsive to treatment with radioactive iodine. The main objective of this study was to examine the possible therapeutic effects of Myricetin on the SW1736 ATC cell line. In this study, we assessed the influence of Myricetin on iodide absorption, sodium iodide symporter gene expression, and apoptosis induction.

MATERIAL METHODS

The interaction between the 7UUY protein of NIS and Myricetin was investigated using AutoDock Vina. Assessment of cell viability was conducted with the MTT assay, whereas cell apoptosis was evaluated by flow cytometry using the Annexin V-FITC Apoptosis Detection kit. A spectrophotometric test based on the Sandell-Kolthoff reaction was conducted to assess the absorption of iodide by SW1736 cells. QRT-PCR analyses were used to assess the expression levels of NIS mRNA in SW1736 cells.

RESULTS

The hydrogen bond interaction pattern created by PyMOL revealed the interactions between the target and ligand molecules. The results demonstrated that Myricetin-induced cell death is dependent on apoptosis in this type of thyroid cancer cell line. QRT-PCR analyses revealed significantly higher NIS mRNA (P < 0.001) levels in the Myricetin-treated group than in the non-treated group. Furthermore, Myricetin treatment significantly increased iodide uptake (P value = 0.0053) in the SW1736 thyroid cancer cell line compared to the control group.

CONCLUSION

These findings suggest that Myricetin has potential as a therapeutic agent by promoting growth inhibition, enhancing NIS gene expression, and increasing iodide uptake in SW1736 cells. Additional research is necessary to clarify the fundamental mechanisms and to evaluate the efficacy of Myricetin in preclinical and clinical settings.