Paclitaxel Inhibits Thyroid Cancer by Regulating AMPK/mTOR and Promoting Ferroptosis

Aim at probe into the mechanisms of paclitaxel inhibition in thyroid cancer. Cell viability was detected via CCK8 assay, KTC-1 proliferation, migration, invasion were detected via colony formation, wound healing as well as transwell assay. Flow cytometry measure the cell cycle and apoptosis, protein expression was detected with Western blot. Iron ions, GSH and MDA were detected by corresponding assay kits, respectively. ROS levels was detected with a fluorescence probe. KTC-1 cells viability decreased significantly when treated with 500 nM paclitaxel, and the proliferation, migration as well as invasion abilities were also significantly weakened. Moreover, paclitaxel induced KTC-1 cell mitosis arrest in G2/M phase to inhibited cell mitosis, and significantly increased the apoptosis. We also found paclitaxel treatment activated AMPK/mTOR signaling pathway, and iron ion, MDA as well as ROS level were significantly increased, while GSH level and expression of GPX4 protein was notably decreased in paclitaxel-treated KTC-1 cells. Our research shows that paclitaxel significantly inhibits the viability, proliferation, migration as well as invasion of KTC-1 cells via activating the AMPK/mTOR signaling pathway, and increase oxidative stress in KTC-1 cells, inducing ferroptosis in KTC-1 cells, providing new support for paclitaxel in the treatment of thyroid cancer.