Apoptotic effects of dehydrocrenatidine via JNK and ERK pathway regulation in oral squamous cell carcinoma

doi:10.1016/j.biopha.2021.111362

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 310902500/23997

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题名:	Apoptotic effects of dehydrocrenatidine via JNK and ERK pathway regulation in oral squamous cell carcinoma
作者:	Ho, HY;Lin, CC;Chuang, YC;Lo, YS;Hsieh, MJ;Chen, MK
关键词:	Dehydrocrenatidine;Oral cancer;Apoptosis;MAPK pathway
日期:	2021
上传时间:	2022-08-05T09:46:12Z (UTC)
出版者:	ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
ISSN:	0753-3322
摘要:	Dehydrocrenatidine, a 8-carboline alkaloid isolated from Picrasma quassioides, has been demonstrated to exert analgesic effects and play essential roles in janus kinase inhibition and exert analgesic effects through the suppression of neuronal excitability. Alkaloids such as paclitaxel and vincristine had been well explored to be chemotherapeutic agents. However, the anticancer effects of dehydrocrenatidine remain unclear. In the present study, we found that dehydrocrenatidine induced apoptosis in human oral cancer cells through both extrinsic and intrinsic pathways involving proteins such as caspase-3, caspase-8, caspase-9, poly (adenosine diphosphateribose) polymerase, and members of the Bcl-2 family. Cotreatment with dehydrocrenatidine and mitogenactivated protein kinase (MAPK) inhibitors indicated that dehydrocrenatidine induced apoptosis through the activation of extracellular signal-regulated kinases (ERK) and c-Jun N-terminal kinases (JNK). The findings provide insight into the potential of dehydrocrenatidine for a new perspective on molecular regulation.
URI:	http://dx.doi.org/10.1016/j.biopha.2021.111362 https://www.webofscience.com/wos/woscc/full-record/WOS:000632077800001 https://ir.csmu.edu.tw:8080/handle/310902500/23997
關聯:	BIOMEDICINE & PHARMACOTHERAPY ,2021,v137
显示于类别:	[中山醫學大學研究成果] 期刊論文

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