Abstract
Objective To investigate the antitumor effect of andrographolide on the ATC cell lines 8505C and CAL62 and to explore the possible mechanism of the effect. Methods CCK8 and colony formation assays were performed to detect proliferation. Cell migration was tested by scratch assay. Annexin V/PI staining was used to detect cell apoptosis and cell cycle. Glucose and lactic acid kits were carried out to evaluate the glycolysis level after andrographolide treatment. Western blot was used to detect the changes in the apoptosis-related proteins and glycolysis-related enzymes in both 8505C and CAL62 cells. Results Treatment with 60 μM andrographolide had significant effects on 8505C and CAL62, including inhibition of proliferation, inhibition of migration, arrest of the cell cycle, promotion of apoptosis, and inhibition of glycolysis. Conclusion Andrographolide has an antitumor effect and can significantly affect glycolysis in ATC cells.
Highlights
Jada et al [16] reported the semisynthesis of andrographolide derivatives and their anticancer activities in vitro, which might be associated with cell cycle progression; ADR reduced VSMC cell proliferation by inducing apoptosis through ceramidep47phox-ROS signaling cascade [17]
Andrographolide has been shown [23] to affect glucose metabolism by targeting Hypoxia-Inducible Factor 1a (HIF-1a), Nuclear Factor Kappa B (NF-kB), MAPK-Src, AP-1, JAK/STAT, Nrf2/keap1, and AMP-Activated Protein Kinase (AMPK) pathway, which may contribute to the effect of andrographolide on inflammation and cancer progression
Glucose is the raw material of the glycolysis pathway, and lactic acid is the product of the glycolysis pathway. e glycolysis pathway of tumor cells consumes a large amount of glucose and produces a large amount of lactic acid at the same time. e results of this study showed that after a certain concentration of andrographolide, the content of glucose and lactic acid in the supernatant of ATC cells remained essentially unchanged from 0 to 48 h, demonstrating that under the action of andrographolide, the glucose in the supernatant of ATC cells is no longer consumed, and the lactic acid content is no longer increased, suggesting that andrographolide can inhibit glycolysis
Summary
To investigate the antitumor effect of andrographolide on the ATC cell lines 8505C and CAL62 and to explore the possible mechanism of the effect. Treatment with 60 μM andrographolide had significant effects on 8505C and CAL62, including inhibition of proliferation, inhibition of migration, arrest of the cell cycle, promotion of apoptosis, and inhibition of glycolysis. Andrographolide has an antitumor effect and can significantly affect glycolysis in ATC cells. Jada et al [16] reported the semisynthesis of andrographolide derivatives and their anticancer activities in vitro, which might be associated with cell cycle progression; ADR reduced VSMC cell proliferation by inducing apoptosis through ceramidep47phox-ROS signaling cascade [17]. Erefore, there is certain research significance in exploring the antitumor activity of andrographolide on ATC cells. Andrographolide has been shown [23] to affect glucose metabolism by targeting Hypoxia-Inducible Factor 1a (HIF-1a), Nuclear Factor Kappa B (NF-kB), MAPK-Src, AP-1, JAK/STAT, Nrf2/keap, and AMP-Activated Protein Kinase (AMPK) pathway, which may contribute to the effect of andrographolide on inflammation and cancer progression. Glycolysis plays a significant role in the occurrence and development of thyroid cancer, especially in ATC. erefore, the study of andrographolide on glycolysis in ATC cells is conducive to the mechanism of andrographolide in ATCs and can provide certain laboratory guidance for the clinical treatment of ATC
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