P110β Inhibition Reduces Histone H3K4 Di-Methylation in Prostate Cancer

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• 作者：Jun Pang ; Yue-Wu Yang ; Yiling Huang ; Jun Yang ; Hao Zhang ; Ruibao Chen ; Liang Dong ; Yan Huang ; Dongying Wang ; Jihong Liu and Benyi Li
• 刊名：The Prostate
• 出版年：2017
• 出版时间：February 15, 2017
• 年：2017
• 卷：77
• 期：3
• 页码：299-308
• 全文大小：10271K
• ISSN：1097-0045

文摘

Epigenetic alteration plays a major role in the development and progression of human cancers, including prostate cancer. Histones are the key factors in modulating gene accessibility to transcription factors and post-translational modification of the histone N-terminal tail including methylation is associated with either transcriptional activation (H3K4me2) or repression (H3K9me3). Furthermore, phosphoinositide 3-kinase (PI3 K) signaling and the androgen receptor (AR) are the key determinants in prostate cancer development and progression. We recently showed that prostate-targeted nano-micelles loaded with PI3 K/p110beta specific inhibitor TGX221 blocked prostate cancer growth in vitro and in vivo. Our objective of this study was to determine the role of PI3 K signaling in histone methylation in prostate cancer, with emphasis on histone H3K4 methylation.