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<p>While the prognosis of thyroid cancer is generally favorable effective therapeutic options remain limited for its advanced or metastatic stages. In this study, we investigated the anti-cancer effects of amiodarone, a widely prescribed anti-arrhythmic agent, in SNU-790 human thyroid cancer cells. Cell viability and cytotoxicity were evaluated using the water-soluble tetrazolium salt-8 assay, which demonstrated a concentration-dependent reduction in cell viability following amiodarone treatment, and the half-maximal inhibitory concentration value was determined accordingly. Flow cytometric analysis revealed that amiodarone induced G1-phase cell-cycle arrest, indicating suppression of thyroid cancer cell proliferation. In addition, a trans-well migration assay showed that amiodarone significantly inhibited cell migration in a concentration-dependent manner, suggesting a potential anti-metastatic effect. Intracellular and mitochondrial reactive oxygen species levels were assessed using 2’,7’-dichlorofluorescein diacetate and MitoSOX™ Red staining, respectively, and both were increased in the amiodarone-treated groups. Additionally, mitochondrial membrane potential was evaluated using JC-10 staining, which revealed a significant decrease. Furthermore, the apoptotic cell population was evaluated by Annexin V/propidium iodide staining, which demonstrated a significant increase in the induction of apoptosis in amiodarone-treated cells. Autophagic responses were further examined by acridine orange staining, which revealed an increase in acidic vesicular organelles, and Western blot analysis confirmed the accumulation of microtubule-associated protein 1 light chain 3B, indicating activation of autophagy in the SNU-790 cells. In conclusion, this study confirmed that amiodarone inhibits the proliferation and migration of thyroid cancer cells and induces apoptosis. Furthermore, we observed that amiodarone induces biochemical changes, including activation of autophagy and mitochondrial dysfunction, suggesting its potential as a repositioned therapeutic agent for thyroid cancer.</p>

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Drug repositioning of amiodarone on the progression of thyroid cancer cells via the induction of apoptosis and autophagy

  • 期刊论文

  • 发表日期：

    2026年6月21日

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  • Taewoong You,
  • Seung-Hyeon Ahn,
  • Hwayoung Na,
  • Dohee Ahn,
  • Hong Kyu Lee,
  • Kyung-Chul Choi

摘要

While the prognosis of thyroid cancer is generally favorable effective therapeutic options remain limited for its advanced or metastatic stages. In this study, we investigated the anti-cancer effects of amiodarone, a widely prescribed anti-arrhythmic agent, in SNU-790 human thyroid cancer cells. Cell viability and cytotoxicity were evaluated using the water-soluble tetrazolium salt-8 assay, which demonstrated a concentration-dependent reduction in cell viability following amiodarone treatment, and the half-maximal inhibitory concentration value was determined accordingly. Flow cytometric analysis revealed that amiodarone induced G1-phase cell-cycle arrest, indicating suppression of thyroid cancer cell proliferation. In addition, a trans-well migration assay showed that amiodarone significantly inhibited cell migration in a concentration-dependent manner, suggesting a potential anti-metastatic effect. Intracellular and mitochondrial reactive oxygen species levels were assessed using 2’,7’-dichlorofluorescein diacetate and MitoSOX™ Red staining, respectively, and both were increased in the amiodarone-treated groups. Additionally, mitochondrial membrane potential was evaluated using JC-10 staining, which revealed a significant decrease. Furthermore, the apoptotic cell population was evaluated by Annexin V/propidium iodide staining, which demonstrated a significant increase in the induction of apoptosis in amiodarone-treated cells. Autophagic responses were further examined by acridine orange staining, which revealed an increase in acidic vesicular organelles, and Western blot analysis confirmed the accumulation of microtubule-associated protein 1 light chain 3B, indicating activation of autophagy in the SNU-790 cells. In conclusion, this study confirmed that amiodarone inhibits the proliferation and migration of thyroid cancer cells and induces apoptosis. Furthermore, we observed that amiodarone induces biochemical changes, including activation of autophagy and mitochondrial dysfunction, suggesting its potential as a repositioned therapeutic agent for thyroid cancer.