Cantharidic acid induces apoptosis in human nasopharyngeal carcinoma cells through p38-mediated upregulation of caspase activation

doi:10.1002/tox.22897

中山醫學大學機構典藏 CSMUIR > 中山醫學大學研究成果 > 期刊論文 > Item 310902500/24300

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/24300

Title:	Cantharidic acid induces apoptosis in human nasopharyngeal carcinoma cells through p38-mediated upregulation of caspase activation
Authors:	Chen, YC;Chen, PN;Lin, CW;Yang, WE;Ho, YT;Yang, SF;Chuang, CY
Keywords:	apoptosis;cantharidic acid;caspase;MAPK;nasopharyngeal carcinoma
Date:	2020
Issue Date:	2022-08-09T08:00:03Z (UTC)
Publisher:	WILEY
ISSN:	1520-4081
Abstract:	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.
URI:	http://dx.doi.org/10.1002/tox.22897 https://www.webofscience.com/wos/woscc/full-record/WOS:000506183900001 https://ir.csmu.edu.tw:8080/handle/310902500/24300
Relation:	ENVIRONMENTAL TOXICOLOGY ,2020 ,v35 ,issue 5 ,p619-627
Appears in Collections:	[中山醫學大學研究成果] 期刊論文

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