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Abstract
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.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
Due to the nature of this research, participants of this study did not agree for their data to be shared publicly, so supporting data is not available.