Background

Current evidence shows that ML385, a new type of nuclear factor erythroid 2-related factor 2 inhibitor, exerts a good inhibitory effect on tumors. However, whether ML385 can regulate the biological behavior of thyroid cancer remains puzzling.

Objectives

We aimed to observe the regulation of ML385 on biological characteristics such as proliferation, apoptosis, migration, and invasion of thyroid tumor cells in vitro and clarify the molecular mechanism of regulating glucose metabolism of tumor cells to lay a foundation for ML385 as a therapeutic tumor drug.

Results

ML385 effectively reduced the viability, proliferation, invasion, migration, glucose consumption, lactate production, adenosine triphosphate level, and extracellular acidification rate of TPC-1 cells and concentration-dependently promoted TPC-1 cell apoptosis, indicating that ML385 inhibited the biological behavior thyroid cancer cell and aerobic glycolysis in vitro. Moreover, the above cellular behaviors were not significantly altered when 2-DG was added to ML385 treatment, suggesting that the inhibition of glycolysis by 2-DG may partially block the effect of ML385 on thyroid cancer cells.

Conclusions

ML385 inhibits the biological behavior of thyroid cancer cells by impairing aerobic glycolysis.

中文翻译：

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ML385 通过损害有氧糖酵解来抑制甲状腺癌细胞的增殖、迁移和侵袭

背景

目前的证据表明，ML385是一种新型核因子红细胞2相关因子2抑制剂，对肿瘤具有良好的抑制作用。然而，ML385是否能够调节甲状腺癌的生物学行为仍然令人费解。

目标

我们的目的是在体外观察ML385对甲状腺肿瘤细胞增殖、凋亡、迁移、侵袭等生物学特性的调节作用，阐明调节肿瘤细胞糖代谢的分子机制，为ML385作为治疗肿瘤药物奠定基础。

结果

ML385有效降低TPC-1细胞的活力、增殖、侵袭、迁移、葡萄糖消耗、乳酸产生、三磷酸腺苷水平和细胞外酸化率，并浓度依赖性促进TPC-1细胞凋亡，表明ML385抑制甲状腺的生物学行为癌细胞和体外有氧糖酵解。此外，当2-DG添加到ML385治疗中时，上述细胞行为没有显着改变，这表明2-DG对糖酵解的抑制可能部分阻断ML385对甲状腺癌细胞的作用。

结论

ML385 通过损害有氧糖酵解来抑制甲状腺癌细胞的生物学行为。