Background

Thyroid cancer is one of the most common malignant tumors of the endocrine system. Studies have demonstrated that maslinic acid (MA) has a wide range of antitumor activities via multiple cellular pathways. However, the role of MA in thyroid cancer remains poorly investigated.

Objective

To investigate the effects and underlying mechanisms of MA on thyroid cancer cells.

Results

MA inhibited cell viability and increased apoptosis in TPC1 and Cal62 cells. MA promoted apoptosis in TPC1 and Cal62 cells in a dose-dependent manner evidenced by flow cytometry and Western blotting. In addition, treatment with MA increased the expression of endoplasmic reticulum (ER) stress markers, such as Binding-immunoglobulin protein (BIP) and C/EBP homologous protein 10 (CHOP), in thyroid cancer cells. In cells treated with 4-phenylbutyric acid, an inhibitor of ER stress, MA-induced apoptosis was partially reversed. Finally, treatment with MA inhibited thyroid cancer growth in a TPC1 cell xenograft model.

Conclusion

Results indicated that MA promoted apoptosis in thyroid cancer cells via ER stress. These findings may provide new insights into novel therapeutic strategies for thyroid cancer.

中文翻译：

---

山楂酸通过内质网应激诱导甲状腺癌细胞凋亡

背景

甲状腺癌是内分泌系统最常见的恶性肿瘤之一。研究表明山楂酸 (MA) 通过多种细胞途径具有广泛的抗肿瘤活性。然而，MA 在甲状腺癌中的作用仍知之甚少。

客观的

探讨MA对甲状腺癌细胞的影响及其潜在机制。

结果

MA 抑制 TPC1 和 Cal62 细胞的细胞活力并增加细胞凋亡。流式细胞术和蛋白质印迹证明，MA 以剂量依赖性方式促进 TPC1 和 Cal62 细胞凋亡。此外，MA治疗增加了甲状腺癌细胞中内质网（ER）应激标记物的表达，例如结合免疫球蛋白（BIP）和C/EBP同源蛋白10（CHOP）。在用 4-苯基丁酸（一种 ER 应激抑制剂）处理的细胞中，MA 诱导的细胞凋亡被部分逆转。最后，在 TPC1 细胞异种移植模型中，MA 治疗抑制了甲状腺癌的生长。

结论

结果表明，MA 通过 ER 应激促进甲状腺癌细胞凋亡。这些发现可能为甲状腺癌的新治疗策略提供新的见解。