Curcumin induces autophagic cell death in human thyroid cancer cells

自噬 姜黄素 甲状腺癌 PI3K/AKT/mTOR通路 程序性细胞死亡 癌细胞 癌症研究 蛋白激酶B 甲状腺间变性癌 化学 癌症 MAPK/ERK通路 细胞生物学 生物 药理学 细胞凋亡 医学 生物化学 信号转导 内科学
作者
Li Zhang,Sheng Xu,Xian Cheng,Jianli Wu,Liying Wu,Yunping Wang,Xiaowen Wang,Jiandong Bao,Huixin Yu
出处
期刊:Toxicology in Vitro [Elsevier]
卷期号:78: 105254-105254 被引量:15
标识
DOI:10.1016/j.tiv.2021.105254
摘要

Curcumin, a polyphenolic compound, is a well-known anticancer agent, although its poor bioavailability remains a big concern. Recent studies suggest that autophagy-targeted therapy may be a useful adjunct treatment for patients with thyroid cancer. Curcumin acts as an autophagy inducer on many cancer cells. However, little is known about the exact role of curcumin on thyroid cancer cells. In the present study, curcumin significantly inhibited the growth of thyroid cancer cells. Autophagy was markedly induced by curcumin treatment as evidenced by an increase in LC3-II conversion, beclin-1 accumulation, p62 degradation as well as the increased formation of acidic vesicular organelles (AVOs). 3-MA, an autophagy inhibitor, partially rescued thyroid cancer cells from curcumin-induced cell death. Additionally, curcumin was found to exert selective cytotoxicity on thyroid cancer cells but not normal epithelial cells and acted as an autophagy inducer through activation of MAPK while inhibition of mTOR pathways. Hyperactivation of the AKT/mTOR axis was observed in the majority of PTC samples we tested, and thyroid cancer cell lines along with cancer tissue specimens sustained a low basal autophagic activity. Taken together, our results provide new evidence that inducing autophagic cell death may serve as a potential anti-cancer strategy to handle thyroid cancer.
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