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2000
Volume 22, Issue 9
  • ISSN: 1871-5206
  • E-ISSN: 1875-5992

Abstract

Background: Anaplastic Thyroid Cancer (ATC) is a rare subtype of thyroid tumors with a high mortality rate. Targeted therapies against ATC are ineffective and mostly transient. Artemisinin has shown excellent anti-tumor activity in several cancers, but its effects on ATC are still unknown. Objective: To evaluate the effects of artemisinin on ATC cells and assess the mechanism underlying drug resistance. Methods: The viability and proliferation rates of the artemisinin-treated CAL-62 and BHT-101 cells were analyzed by MTT and EdU incorporation assays. The protein expression levels were determined by Tandem Mass Tag (TMT) labeling quantitative proteomics and western blotting. Results: Artemisinin treatment significantly decreased the expression levels of COX2 and COX7A2 and increased that of COX14, YEM1l1, ALAS1, and OAT after 48h. In addition, FTL was upregulated in the CAL-62 cells and downregulated in BHT-101 cells. The CAL-62 cells showed transient and reversible resistance to artemisinin, which was correlated to time-dependent changes in HIF1α, PDK1, and PDHA levels. Conclusion: Artemisinin targets the mitochondrial respiratory chain proteins in ATC cells. CAL-62 cells show transient resistance to artemisinin via PDH downregulation, indicating that PDH activation may enhance the cytotoxic effects of artemisinin on ATC cells.

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/content/journals/acamc/10.2174/1871520621666210910100803
2022-05-01
2025-10-07
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/content/journals/acamc/10.2174/1871520621666210910100803
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  • Article Type:
    Research Article
Keyword(s): Anaplastic thyroid cancer; artemisinin; HIF1α; oxidative phosphorylation; PDK1; tolerance
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