Dihydroartemisinin, a potential PTGS1 inhibitor, potentiated cisplatin-induced cell death in non-small cell lung cancer through activating ROS-mediated multiple signaling pathways

doi:10.1016/j.neo.2024.100991

科研成果详情

题名	Dihydroartemisinin, a potential PTGS1 inhibitor, potentiated cisplatin-induced cell death in non-small cell lung cancer through activating ROS-mediated multiple signaling pathways
作者	Ni, Lianli1,2,3; Zhu, Xinping 2; Zhao, Qi1,2; Shen, Yiwei2; Tao, Lu2; Zhang, Ji2; Lin, Han2; Zhuge, Weishan 2; Cho, Young-Chang 3; Cui, Ri1,2; Zhu, Wangyu1,2
发表日期	2024-03-19
发表期刊	Neoplasia (New York, N.Y.) 影响因子和分区
语种	英语
原始文献类型	Journal Article
关键词	Cisplatin Dihydroartemisinin (DHA) Endoplasmic reticulum (ER) stress Mitogen-activated protein kinases (MAPK) Prostaglandin G/H synthase 1 (PTGS1) Reactive oxygen species (ROS)
其他关键词	ER STRESS ; ANGIOGENIC FACTORS ; CYCLOOXYGENASE-1 ; APOPTOSIS ; EXPRESSION ; INDUCTION ; AUTOPHAGY ; TARGET ; COX-1
摘要	Dihydroartemisinin (DHA) exerts an anti-tumor effect in multiple cancers, however, the molecular mechanism of DHA and whether DHA facilitates the anti-tumor efficacy of cisplatin in non-small cell lung cancer (NSCLC) are unclear. Here, we found that DHA potentiated the anti-tumor effects of cisplatin in NSCLC cells by stimulating reactive oxygen species (ROS)-mediated endoplasmic reticulum (ER) stress, C-Jun-amino-terminal kinase (JNK) and p38 MAPK signaling pathways both in vitro and in vivo. Of note, we demonstrated for the first time that DHA inhibits prostaglandin G/H synthase 1 (PTGS1) expression, resulting in enhanced ROS production. Importantly, silencing PTGS1 sensitized DHA-induced cell death by increasing ROS production and activating ER-stress, JNK and p38 MAPK signaling pathways. In summary, our findings provided new experimental basis and therapeutic prospect for the combined therapy with DHA and cisplatin in some NSCLC patients.
资助项目	National Natural Science Foundation of China [81672305]; Health Commission of Zhejiang Province [2022RC292]; Natural Science Foundation of Zhejiang Province
出版者	Elsevier Inc.
ISSN	1476-5586
EISSN	1476-5586
卷号	51
DOI	10.1016/j.neo.2024.100991
页数	15
WOS类目	Oncology
WOS研究方向	Oncology
WOS记录号	WOS:001291566700001
收录类别	PUBMED ; SCOPUS ; SCIE
URL	查看原文
PubMed ID	38507887
SCOPUSEID	2-s2.0-85188453510
通讯作者地址	[Zhu, Wangyu]Cellular and Molecular Biology Laboratory,Affiliated Zhoushan Hospital of Wenzhou Medical University,Zhejiang,Zhoushan,316020,China ; [Cui, Ri]Cancer and Anticancer Drug Research Center,School of Pharmaceutical Sciences,Wenzhou Medical University,Building 11, Chashan Street, University Town, Zhejiang,Wenzhou,325035,China ; [Cho, Young-Chang]Research Institute of Pharmaceutical Sciences,College of Pharmacy,Chonnam National University,Gwangju,61186,South Korea
Scopus学科分类	Cancer Research
引用统计
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/210331
专题	药学院（分析测试中心）其他_附属舟山医院（舟山医院）
通讯作者	Cho, Young-Chang; Cui, Ri; Zhu, Wangyu
作者单位	1.Cellular and Molecular Biology Laboratory,Affiliated Zhoushan Hospital of Wenzhou Medical University,Zhejiang,Zhoushan,316020,China; 2.Cancer and Anticancer Drug Research Center,School of Pharmaceutical Sciences,Wenzhou Medical University,Zhejiang,Wenzhou,325035,China; 3.Research Institute of Pharmaceutical Sciences,College of Pharmacy,Chonnam National University,Gwangju,61186,South Korea
第一作者单位	附属舟山医院（舟山医院）; 药学院（分析测试中心）
通讯作者单位	附属舟山医院（舟山医院）; 药学院（分析测试中心）
第一作者的第一单位	附属舟山医院（舟山医院）
推荐引用方式 GB/T 7714	Ni, Lianli,Zhu, Xinping,Zhao, Qi,et al. Dihydroartemisinin, a potential PTGS1 inhibitor, potentiated cisplatin-induced cell death in non-small cell lung cancer through activating ROS-mediated multiple signaling pathways[J]. Neoplasia (New York, N.Y.),2024,51.
APA	Ni, Lianli., Zhu, Xinping., Zhao, Qi., Shen, Yiwei., Tao, Lu., ... & Zhu, Wangyu. (2024). Dihydroartemisinin, a potential PTGS1 inhibitor, potentiated cisplatin-induced cell death in non-small cell lung cancer through activating ROS-mediated multiple signaling pathways. Neoplasia (New York, N.Y.), 51.
MLA	Ni, Lianli,et al."Dihydroartemisinin, a potential PTGS1 inhibitor, potentiated cisplatin-induced cell death in non-small cell lung cancer through activating ROS-mediated multiple signaling pathways".Neoplasia (New York, N.Y.) 51(2024).