Maslinic acid induces apoptosis in thyroid cancer cells via endoplasmic reticulum stress

IF 1.1 4区医学 Q4 TOXICOLOGY

Molecular & Cellular Toxicology Pub Date : 2023-12-12 DOI:10.1007/s13273-023-00406-6

Jing Zhu, Pinghui Tu, Yu Yang, Dandan Zhang, Fengling Chen

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Abstract

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.

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马钱子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，马斯林酸（MA）通过多种细胞途径具有广泛的抗肿瘤活性。结果MA抑制TPC1和Cal62细胞的存活率并增加其凋亡。流式细胞术和 Western 印迹分析表明，MA 对 TPC1 和 Cal62 细胞凋亡的促进作用呈剂量依赖性。此外，MA还能增加甲状腺癌细胞内质网（ER）应激标记物的表达，如结合免疫球蛋白蛋白（BIP）和C/EBP同源蛋白10（CHOP）。在用ER应激抑制剂4-苯基丁酸处理的细胞中，MA诱导的细胞凋亡被部分逆转。结论研究结果表明，MA能通过ER应激促进甲状腺癌细胞凋亡。这些发现为甲状腺癌的新型治疗策略提供了新的思路。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Molecular & Cellular Toxicology 医学-毒理学

CiteScore

2.50

自引率

17.60%

发文量

114

审稿时长

6-12 weeks

期刊介绍： Molecular & Cellular Toxicology publishes original research and reviews in all areas of the complex interaction between the cell´s genome (the sum of all genes within the chromosome), chemicals in the environment, and disease. Acceptable manuscripts are the ones that deal with some topics of environmental contaminants, including those that lie in the domains of analytical chemistry, biochemistry, pharmacology and toxicology with the aspects of molecular and cellular levels. Emphasis will be placed on toxic effects observed at relevant genomics and proteomics, which have direct impact on drug development, environment health, food safety, preventive medicine, and forensic medicine. The journal is committed to rapid peer review to ensure the publication of highest quality original research and timely news and review articles.