Cantharidic acid (CA) is the hydrolysis product of the acid anhydride cantharidin, which is a natural toxin secreted by several species of blister beetles. Several studies have indicated that as an inhibitor of protein phosphatase 2 (PP2A), CA induces apoptosis in various human cancer cells. However, the effect of CA on human nasopharyngeal carcinoma (NPC) cells and the underlying pathways have not been addressed. In our current study, we tested the hypothesis that CA treatment reduces the viability of human NPC cells (HONE‐1, NPC‐39, and NPC‐BM) by inducing apoptosis. Results indicated that CA markedly reduced cell viability, which was revealed by the upregulation of caspase activation in extrinsic and intrinsic apoptosis pathways as well as the upregulation of extracellular‐signal‐regulated kinase 1/2 (ERK1/2), p38, and c‐Jun N‐terminal kinase 1/2 (JNK1/2) pathways. Coadministration of a p38 inhibitor (SB203580) with CA abolished the activation of caspase proteins. These findings indicated that CA treatment leads to apoptosis in human NPC cells through the upregulation of caspase activation, mediated particularly by the p38 pathway. Hence, CA is a promising therapeutic agent for human NPC.

中文翻译：

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斑蝥酸通过 p38 介导的半胱天冬酶激活上调诱导人鼻咽癌细胞凋亡

斑蝥酸 (CA) 是酸酐斑蝥素的水解产物，斑蝥素是几种水疱甲虫分泌的天然毒素。多项研究表明，作为蛋白磷酸酶 2 (PP2A) 的抑制剂，CA 诱导多种人类癌细胞凋亡。然而，CA 对人鼻咽癌 (NPC) 细胞和潜在途径的影响尚未得到解决。在我们目前的研究中，我们检验了 CA 治疗通过诱导细胞凋亡降低人类 NPC 细胞（HONE-1、NPC-39 和 NPC-BM）活力的假设。结果表明，CA 显着降低细胞活力，这通过外在和内在细胞凋亡途径中 caspase 激活的上调以及细胞外信号调节激酶 1/2 (ERK1/2)、p38、和 c-Jun N 端激酶 1/2 (JNK1/2) 通路。p38 抑制剂 (SB203580) 与 CA 的共同给药消除了半胱天冬酶蛋白的激活。这些发现表明，CA 治疗通过上调半胱天冬酶激活导致人 NPC 细胞凋亡，尤其是由 p38 途径介导。因此，CA 是一种很有前途的人类 NPC 治疗剂。