Abstract
Objective This study aimed to explore the mechanism of triptolide (TPL) in the treatment of thyroid cancer (TC).Methods The targets of TPL in TC were collected from databases. A protein-protein interaction network was constructed using the common targets of TPL and TC. Enrichment analysis was performed using the DAVID database. The effects of TPL on cell activity, apoptosis, and cell cycle were assessed using CCK-8 assay and flow cytometry. Western blot analysis was conducted to measure the levels of caspase 3, caspase 7, PCNA, ki67, cleaved caspase 7, cleaved caspase 3, and p-P53. RT-PCR was used to measure TP53 mRNA levels.Results The protein-protein interaction network revealed 8 potential targets for TPL in TC treatment. Enrichment analysis indicated that TPL mainly involved in cell apoptosis, proliferation, and inflammation response. In vitro studies showed that TPL inhibited K1 cell activity, down-regulated PCNA and ki67 levels, and up-regulated caspase 3, caspase 7, cleaved caspase 3, cleaved caspase 7, p-P53 protein expressions, and TP53 mRNA levels. TPL also promoted K1 cell apoptosis and arrested cell cycle at the G2/M and S phase.Conclusion TPL exhibits antitumor effects on K1 cells by inhibiting cell proliferation, inducing cell apoptosis, and disrupting cell cycle.