Cordycepin Induces Apoptosis of CGTH W-2 Thyroid Carcinoma Cells through the Calcium−Calpain−Caspase 7-PARP Pathway

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• 作者：Ying Chen ; Yung-Chia Chen ; Yen-Tung Lin ; Shih-Horng Huang ; Seu-Mei Wang
• 刊名：Journal of Agricultural and Food Chemistry
• 出版年：2010
• 出版时间：November 24, 2010
• 年：2010
• 卷：58
• 期：22
• 页码：11645-11652
• 全文大小：1004K
• 年卷期：v.58,no.22(November 24, 2010)
• ISSN：1520-5118

文摘

Cordycepin, a nucleoside isolated from Cordyceps sinensis, is an inhibitor of polyadenylation and has an antitumor effect. We used CGTH W-2, a follicular thyroid carcinoma cell line, to study the mechanism of the anticancer effect of cordycepin. Cordycepin decreased cell viability and resulted in apoptosis but not necrosis. Cordycepin increased intracellular calcium levels triggering calpain activation, which led to apoptosis. BAPTA/AM and calpeptin inhibited the cordycepin-induced cleavage of caspase 7 and poly (ADP-ribose) polymerase (PARP), implying an upstream role of calcium and calpain. CGTH W-2 cells expressed four subtypes of adenosine receptors (AR), A₁AR, A_2AAR, A_2BAR, and A₃AR. Specific antagonists to AR subtypes all blocked cordycepin-induced apoptosis to different degrees. Small interfering RNA for A₁AR and A₃AR abrogated cordycepin-induced apoptosis. In conclusion, the cordycepin-induced apoptosis of CGTH W-2 cells is mediated by the calcium−calpain−caspase 7-PARP pathway, and ARs are involved in the apoptotic effect of cordycepin.

Keywords (keywords):

Cordycepin; thyroid carcinoma cells; apoptosis; signaling mechanism