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Triptolide induces apoptosis in human anaplastic thyroid carcinoma cells by a p53-independent but NF-kappaB-related mechanism. Oncology reports [Oncol Rep] Journal article

 
Zhu W, Hu H, Qiu P, Yan G 
Triptolide induces apoptosis in human anaplastic thyroid carcinoma cells by a p53-independent but NF-kappaB-related mechanism. [JOURNAL ARTICLE]
Oncol Rep 2009 Dec; 22(6):1397-1401.


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 kappaB (NF-kappaB) pathway. Our studies suggest that triptolide functions as an effective apoptotic inducer in a p53-independent, but NF-kappaB-dependent mechanism, thus providing a promising agent for tumor types with p53 mutation/deletion.



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