Radiotherapy (RT) is one of the key treatments for thyroid cancer (TC). Our previous results showed that RT enhances autophagy and blocks RT-induced P53-dependent TC cell apoptosis. However, how RT induces autophagy in TC remains poorly understood. Human TC cell lines, SW579 cells (primary squamous cell carcinoma cells) and FTC-133 (follicular thyroid carcinoma cells) and were used to expose to X-ray irradiation. The relationships between reactive oxygen species (ROS), apoptosis, and autophagy were analyzed by FACS in TC cells. In X-ray-treated TC cells, the proportion of 2’, 7’–dichlorofluorescein (DCF)-positive cells indicating intracellular ROS levels were significantly higher. X-ray irradiation reduced superoxide dismutase (SOD) activity in SW579 cells. The ROS scavengers N-acetyl-L-cysteine (NAC) and SOD enhanced X-ray-induced apoptosis via blocking PI3K-Akt-dependent autophagy in TC cells. ROS mediate the induction of PI3K–Akt-dependent protective autophagy by RT in TC cells.

放射治疗（RT）是甲状腺癌（TC）的主要治疗方法之一。我们以前的结果表明RT增强自噬并阻断RT诱导的P53依赖性TC细胞凋亡。然而，如何RT诱导TC自噬尚不清楚。人TC细胞系，SW579细胞（原发性鳞状细胞癌细胞）和FTC-133（卵泡状甲状腺癌细胞）被用于暴露于X射线照射。FACS分析了TC细胞中活性氧（ROS），凋亡和自噬之间的关系。在经过X射线处理的TC细胞中，表明细胞内ROS水平的2'，7'-二氯荧光素（DCF）阳性细胞比例显着更高。X射线照射降低了SW579细胞中的超氧化物歧化酶（SOD）活性。ROS清除剂N-乙酰基-L-半胱氨酸（NAC）和SOD通过阻断TC细胞中PI3K-Akt依赖性自噬增强X射线诱导的细胞凋亡。ROS通过RT介导TC细胞中PI3K–Akt依赖性保护性自噬的诱导。