Heydarzadeh Shabnam, Moshtaghie Ali Asghar, Daneshpour Maryam, Pishdad Reza, Farahani Amin, Hedayati Mehdi
Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Biochemistry, Falavarjan Branch, Islamic Azad University, Isfahan, Iran.
Food Chem Toxicol. 2025 Jan;195:115137. doi: 10.1016/j.fct.2024.115137. Epub 2024 Nov 23.
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.
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.
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.
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.
间变性甲状腺癌细胞缺乏有效摄取碘的能力，因此对放射性碘治疗无反应。本研究的主要目的是检测杨梅素对SW1736人间变性甲状腺癌细胞系的潜在治疗作用。在本研究中，我们评估了杨梅素对碘摄取、碘化钠同向转运体基因表达和细胞凋亡诱导的影响。
使用AutoDock Vina研究NIS的7UUY蛋白与杨梅素之间的相互作用。采用MTT法评估细胞活力，而使用Annexin V-FITC凋亡检测试剂盒通过流式细胞术评估细胞凋亡。基于桑德尔-科尔托夫反应进行分光光度测试，以评估SW1736细胞对碘的摄取。采用实时定量聚合酶链反应（QRT-PCR）分析评估SW1736细胞中NIS mRNA的表达水平。
PyMOL生成的氢键相互作用模式揭示了靶标与配体分子之间的相互作用。结果表明，在这种类型的甲状腺癌细胞系中，杨梅素诱导的细胞死亡依赖于细胞凋亡。QRT-PCR分析显示，杨梅素处理组的NIS mRNA水平（P < 0.001）显著高于未处理组。此外，与对照组相比，杨梅素处理显著增加了SW1736甲状腺癌细胞系中的碘摄取（P值 = 0.0053）。
这些发现表明，杨梅素具有作为治疗剂的潜力，可通过促进生长抑制、增强NIS基因表达以及增加SW1736细胞中的碘摄取来发挥作用。需要进一步的研究来阐明其基本机制，并评估杨梅素在临床前和临床环境中的疗效。
