Triptolide induces apoptosis in human anaplastic thyroid carcinoma cells by a p53-independent but NF-κB-related mechanism
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- Published online on: December 1, 2009 https://doi.org/10.3892/or_00000580
- Pages: 1397-1401
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Abstract
Triptolide, a traditional anti-inflammatory and anti-immunodepressive agent, has been reported to exert anti-neoplastic activity on several human tumor cell lines. This study investigates the pro-apoptotic function and the functional mechanism of triptolide on anaplastic thyroid carcinoma (ATC) cells. Experiments presented here demonstrated that triptolide had dose-dependent effects on cell viability of human ATC cell line TA-K cells through inducing cell apoptosis. In the molecular level, triptolide did not successfully initiate p53 signaling pathway, but downregulated the nuclear factor κB (NF-κB) pathway. Our studies suggest that triptolide functions as an effective apoptotic inducer in a p53-independent, but NF-κB-dependent mechanism, thus providing a promising agent for tumor types with p53 mutation/deletion.