Dehydrocrenatidine extracted from Picrasma quassioides induces the apoptosis of nasopharyngeal carcinoma cells through the JNK and ERK signaling pathways

doi:10.3892/or.2021.8117

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 310902500/23411

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/23411

Title:	Dehydrocrenatidine extracted from Picrasma quassioides induces the apoptosis of nasopharyngeal carcinoma cells through the JNK and ERK signaling pathways
Authors:	Hsieh, MC;Lo, YS;Chuang, YC;Lin, CC;Ho, HY;Hsieh, MJ;Lin, JT
Keywords:	dehydrocrenatidine;nasopharyngeal cancer;apoptosis;MAPK pathway
Date:	2021
Issue Date:	2022-08-05T09:36:51Z (UTC)
Publisher:	SPANDIDOS PUBL LTD
ISSN:	1021-335X
Abstract:	Nasopharyngeal carcinoma (NPC) is an indicator disease in Asia due to its unique geographical and ethnic distribution. Dehydrocrenatidine (DC) is a beta-carboline alkaloid abundantly present in Picrasma quassioides (D. Don) Benn, a deciduous shrub or small tree native to temperate regions of southern Asia, and beta-carboline alkaloids play anti-inflammatory and antiproliferative roles in various cancers. However, the mechanism and function of DC in human NPC cells remain only partially explored. The present study aimed to examine the cytotoxicity and biochemical role of DC in human NPC cells. The MTT method, cell cycle analysis, DAPI determination, Annexin V/PI double staining, and mitochondrial membrane potential examination were performed to evaluate the effects of DC treatment on human NPC cell lines. In addition, western blotting analysis was used to explore the effect of DC on apoptosis and signaling pathways in related proteins. The analysis results confirmed that DC significantly reduced the viability of NPC cell lines in a dose- and time-dependent manner and induced apoptosis through internal and external apoptotic pathways (including cell cycle arrest, altered mitochondrial membrane potential, and activated death receptors). Western blot analysis illustrated that DC's effect on related proteins in the mitogen-activated protein kinase pathway can induce apoptosis by enhancing ERK phosphorylation and inhibiting Janus kinase (JNK) phosphorylation. Notably, DC induced apoptosis by affecting the phosphorylation of JNK and ERK, and DC and inhibitors (SP600125 and U0126) in combination restored the overexpression of p-JNK and p-ERK. To date, this is the first study to confirm the apoptosis pathway induced by DC phosphorylation of p-JNK and p-REK in human NPC. On the basis of evidence obtained from this study, DC targeting the inhibition of NPC cell lines may be a promising future strategy for NPC treatment.
URI:	http://dx.doi.org/10.3892/or.2021.8117 https://www.webofscience.com/wos/woscc/full-record/WOS:000665024300001 https://ir.csmu.edu.tw:8080/handle/310902500/23411
Relation:	ONCOLOGY REPORTS ,2021,v46,issue 2
Appears in Collections:	[中山醫學大學研究成果] 期刊論文

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