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Archive > Volume 30 Issue 3 > 2023,30(3):211-216. DOI:10.3872/j.issn.1007-385X.2023.03.004 Prev Next
Basic Research
Amentoflavone induces apoptosis and suppresses proliferation of thyroid carcinoma SW579 cells by inhibiting the activation of JAK2-STAT3 pathway
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Abstract:
Objective: To investigate the effects of Amentoflavone (AF) on the JAK2-STAT3 pathway activation, apoptosis，and proliferation of thyroid carcinoma SW579 cells. Methods: SW579 cells were treated with AF at different concentrations (0，50, 100, 150, and 200 μmol/L) for 24 h, 48 h, and 72 h, respectively. Then, the effects of AF on the proliferation and apoptosis of SW579 cells were detected by CCK-8 and Celigo cell count and FCM, respectively; and the effects of AF on the JAK2-STAT3 pathway activation and the mRNA and protein expression of its downstream genes c-Myc, Bcl2 and Survivin in SW579 cells were detected by qPCR and Western blotting. Results: After the treatment with AF, the proliferation of SW579 cells was suppressed significantly while the apoptosis was promoted significantly, which were all in a dose-dependent manner (both P<0.05). The activation of JAK2-STAT3 pathway was significantly inhibited (P<0.05), and the mRNA and protein expression of the downstream genes c-Myc, Bcl2, and survivin in SW579 cells was significantly decreased (all P<0.05) after the treatment with AF. Conclusion: AF may contribute to apoptosis induction and proliferation suppression of thyroid carcinoma SW579 cells via inhibiting the activation of JAK2-STAT3 pathway and its downstream gene expression. AF has the potential to serve as a novel therapeutic approach for the management of thyroid carcinoma.
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