[PHI对Molt-4细胞组蛋白甲基化和乙酰化影响的实验研究]
[Experiment study of PHI on histone methylation and acetylation in Molt-4 cells].
作者信息
Huang Yi-Qun, Ma Xu-Dong, Zhen Rui-Ji, Chiao Jen-Wei, Liu De-Long
机构信息
Department of Hematology, Zhangzhou Municipal Hospital, Fujian Medical University, Zhangzhou 363000, China.
出版信息
Zhonghua Xue Ye Xue Za Zhi. 2007 Sep;28(9):612-5.
OBJECTIVE
To investigate the effect of phenyl-hexyl isothiocyanate (PHI) on acetylation and methylation of histone in acute lymphoblastic leukemia cell line Molt4.
METHODS
The inhibition of cell proliferation was observed by MTT method and clone suppression test. Apoptosis and cell cycle arrest were measured by flow cytometry. The alterations in histone acetyltransferase and acetylation and methylation of histones were detected by Western blot.
RESULTS
PHI could up-regulate the expression of acetyltransferase (P300/CBP), markedly induced the accumulation of acetylated histone H3, H4 and methylated histone H3 lysine 4 (H3K4), and inhibited methylation on lysine 9 of H3 (H3K9). The epigenetic regulation resulted in cell cycle arrest at G0/G1 phase, and induction of apoptosis.
CONCLUSIONS
PHI can modulate both histone methylation and acetylation. It may serve as a histone deacetylase inhibitor, and might be a potential novel anti-leukemia agent.
目的
研究苯基己基异硫氰酸酯（PHI）对急性淋巴细胞白血病细胞系Molt4组蛋白乙酰化和甲基化的影响。
方法
采用MTT法和克隆抑制试验观察细胞增殖抑制情况。通过流式细胞术检测细胞凋亡和细胞周期阻滞。采用蛋白质免疫印迹法检测组蛋白乙酰转移酶以及组蛋白乙酰化和甲基化的变化。
结果
PHI可上调乙酰转移酶（P300/CBP）的表达，显著诱导乙酰化组蛋白H3、H4以及甲基化组蛋白H3赖氨酸4（H3K4）的积累，并抑制H3赖氨酸9（H3K9）的甲基化。这种表观遗传调控导致细胞周期阻滞于G0/G1期，并诱导细胞凋亡。
结论
PHI可调节组蛋白甲基化和乙酰化。它可能作为一种组蛋白去乙酰化酶抑制剂，或许是一种潜在的新型抗白血病药物。
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