MDM2-MOF-H4K16ac axis contributes to tumorigenesis induced by Notch
MDM2-MOF-H4K16ac axis contributes to tumorigenesis induced by Notch
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DOI：
10.1111/febs.12863
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发表时间：
2014-08-01
期刊：
影响因子：
5.4
通讯作者：
Zhang, Jing-Hua
中科院分区：
文献类型：
--
作者：
Liu, Yan;Xing, Zhao-Bin;Zhang, Jing-Hua
识别参与Notch信号传递的表观遗传机制对于个体化药物是有用的。我们观察到，在肝细胞癌和乳腺癌细胞系和组织中，异常高水平的Notch活性导致H4K16ac下调。这种下调的乙酰化是男性在不同癌症类型中全长小鼠双分钟2上调后第一次降解增加的结果。我们观察到，第一次增加男性可以减弱由异常高水平的Notch活性引起的异质性。我们的结果为分析和治疗Notch诱导的肝细胞癌和乳腺癌提供了新的见解。
Identification of the epigenetic mechanisms involved in the transmission of Notch signaling is useful for personalized medicine. We observed that aberrantly high levels of Notch activity resulted in H4K16ac downregulation in hepatocellular carcinoma and breast cancer cell lines and tissues. This downregulated acetylation was a consequence of increased male on the first degradation following the upregulation of full-length murine double minute 2 in different cancer types. We observed that increases in male on the first could attenuate heterogeneity induced by aberrantly high levels of Notch activity. Our results provide new insights into the analysis and treatment of Notch-induced hepatocellular carcinoma and breast cancer.