文献类型：期刊文献

英文题名：Downregulation of PRMT5 by AMI-1 enhances therapeutic efficacy of compound kushen injection in lung carcinoma in vitro and in vivo

作者：Yang, Ruiying[1];Dong, Shuhong[1];Zhang, Jinghui[2];Zhu, Shihao[1];Miao, Guoliang[1];Zhang, Baolai[1]

第一作者：Yang, Ruiying

通信作者：Zhang, BL[1]

机构：[1]Lanzhou Univ, Sch Basic Med Sci, Dept Pharmacol, Lanzhou 730000, Peoples R China;[2]Gansu Univ Tradit Chinese Med, Coll Pharm, Lanzhou 730000, Gansu, Peoples R China

第一机构：Lanzhou Univ, Sch Basic Med Sci, Dept Pharmacol, Lanzhou 730000, Peoples R China

通信机构：[1]corresponding author), Lanzhou Univ, Sch Basic Med Sci, Dept Pharmacol, Lanzhou 730000, Peoples R China.

年份：2023

卷号：478

期号：5

起止页码：1031

外文期刊名：MOLECULAR AND CELLULAR BIOCHEMISTRY

收录：;Scopus(收录号：2-s2.0-85139553270);WOS:【SCI-EXPANDED(收录号:WOS:000865686400001)】；

语种：英文

外文关键词：Compound Kushen injection; AMI-1; PRMT5; eIF4E; Lung carcinoma

摘要：Protein arginine methyltransferase 5 (PRMT5) is overexpressed in lung carcinoma, which promotes tumor cell proliferation, survival, migration and invasion. Compound Kushen injection (CKI) is a mixture of natural compounds extracted from Kushen and Baituling, which are mainly used to stop in cancer pain and bleeding. Here we found that cell viability and colony formation were inhibited after the incubation of AMI-1. Meanwhile, AMI-1 suppressed cell migration, enhanced apoptosis, induced cell cycle arrest, inhibited PRMT5 expression and histone H3R8 and H4R3 symmetric di-methylation (H3R8me2s and H4R3me2s) accumulation, down-regulated the expression of eukaryotic translation initiation factor 4E (eIF4E) in lung carcinoma cells. Moreover, AMI-1 suppressed tumor growth, decreased H3R8me2s and H4R3me2s accumulation, down-regulated eIF4E expression and increased p53 expression in lung carcinoma xenografts of BALB/c nude mice. Of note, combined and CKI markedly enhanced the anticancer efficacy CKI in lung carcinoma. The above findings demonstrated that AMI-1 has established antineoplastic activity and this role may be associated with affecting the function of eIF4E via inhibiting PRMT5 activity or protein levels in lung carcinoma. This study highlights evidence of novel selective anticancer activity of AMI-1 in combination with CKI in lung carcinoma.