Re-evaluation of the role of autophagy in thyroid cancer treatment
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- Kazakova Darya
- Department of Molecular Medicine, Atomic Bomb Disease Institute and Nagasaki University of Graduate School of Biosciences, Nagasaki 852-8523, Japan
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- Shimamura Mika
- Department of Molecular Medicine, Atomic Bomb Disease Institute and Nagasaki University of Graduate School of Biosciences, Nagasaki 852-8523, Japan
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- Kurashige Tomomi
- Department of Molecular Medicine, Atomic Bomb Disease Institute and Nagasaki University of Graduate School of Biosciences, Nagasaki 852-8523, Japan
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- Hamada Koichiro
- Department of Molecular Medicine, Atomic Bomb Disease Institute and Nagasaki University of Graduate School of Biosciences, Nagasaki 852-8523, Japan Department of General Medicine, Nagasaki University of Graduate School of Biosciences, Nagasaki 852-8523, Japan
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- Nagayama Yuji
- Department of Molecular Medicine, Atomic Bomb Disease Institute and Nagasaki University of Graduate School of Biosciences, Nagasaki 852-8523, Japan
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Abstract
<p>Numerous studies have examined the role of autophagy in thyroid cancer treatment; however there are discrepancies among the reported data, with some showing the pro-survival and others the anti-survival effects of autophagy. These discrepant results appear to be at least in part due to insufficient analyses or data misinterpretation as well as improper assessments of autophagic activity. Therefore, the present study re-evaluated the regulation of autophagic activity by various anticancer modalities and examined the role of autophagy in thyroid cancer treatment in three thyroid cancer cell lines (TPC1, ACT1 and KTC1). The immunofluorescence and DalGreen findings demonstrated that cisplatin, irradiation and sorafenib were all autophagy inducers as previously reported, but, unlike previous studies using thyroid cancer cells, doxorubicin acted as an inhibitor. KTC1 cells are unique because they only responded to cisplatin. The efficacy of anticancer therapeutics was significantly higher in chloroquine or 3-methyladenine-treated autophagy-defective cells than in autophagy-competent cells, thereby indicating the pro-survival effect of autophagy induced by anticancer therapeutics, which is partly due to inhibition of apoptosis. Thus, the present findings relating to several anticancer therapeutics and three thyroid cancer cell lines demonstrate the pro-survival effect of autophagy in thyroid cancer treatment. Although the present study only involved cell lines, it provides evidence for the beneficial combination of the anticancer therapeutic modalities with autophagy inhibitors, and proposes that autophagy inhibitors may serve as a possible adjunctive therapy for thyroid cancer.</p>
Journal
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- Endocrine Journal
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Endocrine Journal 69 (7), 847-862, 2022
The Japan Endocrine Society