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Triptolide‐Induced Apoptosis of Androgen‐Independent Prostatic Cancer ( AIPC ) via Modulation of Histone Methylation
Author(s) -
Zhao Kailiang,
Wang Weixing,
Yu Xiaohui,
Zhou Xing,
Shi Qiao,
Hu Yunfei
Publication year - 2012
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.21011
Subject(s) - triptolide , ezh2 , cancer research , pharmacology , epigenetic therapy , histone methylation , downregulation and upregulation , methylation , apoptosis , chemistry , epigenetics , prostate cancer , cancer , medicine , dna methylation , biochemistry , gene expression , gene
trategy, Management and Health Policy Enabling Technology, Genomics, Proteomics Preclinical Research Preclinical Development Toxicology, Formulation Drug Delivery, Pharmacokinetics Clinical Development Phases I‐III Regulatory, Quality, Manufacturing Postmarketing Phase IVTriptolide is the principal active ingredient in extracts from the C hinese herb, T ripterygium wilfordii H ook. F ( TwHF ) and has various biological functions including immunosuppression, anti‐inflammatory, antiviral, and antitumor properties. Triptolide has antitumor activity in a variety of tumors, and numerous studies have attempted to elucidate the potential antitumor mechanism. Triptolide can modulate histone methylation, suggesting that epigenetic mechanisms may play an important role in its antitumor activity. The present study assessed the association between the antitumor effects of triptolide in androgen‐independent prostatic cancer and the regulation of histone methylation. Triptolide inhibited the proliferation of the androgen‐independent prostatic cancer cell line, Du 145 and induced apoptosis in a time‐ and dose‐dependent manner. Triptolide decreased histone H3K27me3 methylation via downregulation of histone methyltransferase enhancer of zeste 2, which may represent the antitumor mechanism of triptolide.