ZBP-89 enhances Bak expression and causes apoptosis in hepatocellular carcinoma cells.
ZBP-89 enhances Bak expression and causes apoptosis in hepatocellular carcinoma cells.
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DOI：
10.1016/j.bbamcr.2010.09.005
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发表时间：
2011-01
期刊：
影响因子：
--
通讯作者：
Lai PB
中科院分区：
文献类型：
--
作者：
To AK;Chen GG;Chan UP;Ye C;Yun JP;Ho RL;Tessier A;Merchant JL;Lai PB
ZBP-89能增强肿瘤细胞对死亡的刺激。然而，导致ZBP-89抑制作用的分子机制尚不清楚。本研究以4种肝细胞系为研究对象，筛选ZBP-89在细胞死亡途径中的作用靶点。进一步分析鉴定的巴克在ZBP-89介导的细胞凋亡中的作用。结果表明，ZBP-89可明显诱导细胞凋亡，并呈时间依赖性。它显著上调促凋亡巴克的水平。根据巴克启动子荧光素酶报告基因分析和电泳迁移率变动分析的结果，ZBP-89靶向人巴克启动子-457和-407之间的区域以刺激巴克表达。ZBP-89诱导的巴克增加和ZBP-89介导的凋亡被巴克siRNA显著抑制，证实巴克被ZBP-89特异性靶向以促进凋亡。本研究表明ZBP-89通过促进巴克蛋白水平的升高而诱导肝癌细胞凋亡。
ZBP-89 can enhance tumor cells to death stimuli. However, the molecular mechanism leading to the inhibitory effect of ZBP-89 is unknown. In this study, 4 liver cell lines were used to screen for the target of ZBP-89 on cell death pathway. The identified Bak was further analyzed for its role in ZBP-89-mediated apoptosis. The result showed that ZBP-89 significantly and time-dependently induced apoptosis. It significantly upregulated the level of pro-apoptotic Bak. ZBP-89 targeted a region between -457 and -407 of human Bak promoter to stimulate Bak expression based on the findings of Bak promoter luciferase report gene assay and electrophoretic mobility shift assay. ZBP-89-induced Bak increase and ZBP-89-mediated apoptosis were markedly suppressed by Bak siRNA, confirming that Bak was specifically targeted by ZBP-89 to facilitate apoptosis. In conclusion, this study demonstrated that ZBP-89 significantly induced apoptosis of HCC cells via promoting Bak level.
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影响因子：
9.7
作者：
Chen, George G.;Chan, Ursula P. F.;Bai, Long-Chuan;Fung, King Yip;Tessier, Art;To, Ann K. Y.;Merchant, Juanita L.;Lai, Paul B. S.
通讯作者：
Lai, Paul B. S.
影响因子：
4.8
作者：
Law, GL;Itoh, H;Morris, DR
通讯作者：
Morris, DR
影响因子：
4.6
作者：
Li, Xiangen;Xiong, Jing-Wei;Arnaout, M. Amin
通讯作者：
Arnaout, M. Amin
影响因子：
4
作者：
Hu, RG;Zhai, QW;Liu, XY
通讯作者：
Liu, XY
影响因子：
2.1
作者：
Wu, Yongzhong;Zhang, Xueping;Zehner, Zendra E.
通讯作者：
Zehner, Zendra E.