脱磷
蛋白磷酸酶2
磷酸化
癌症研究
基因敲除
细胞生物学
细胞凋亡
生物
化学
磷酸酶
生物化学
作者
Xinzhou Yang,Lang Zhang,Shanqing Jiang,Zhuo Cheng,Guan Wang,Xu Huang
出处
期刊:Oncotarget
[Impact Journals, LLC]
日期:2016-05-26
卷期号:7 (26): 40285-40296
被引量:21
标识
DOI:10.18632/oncotarget.9603
摘要
Our previous study discovered that isoliensinine (isolie) triggers hepatocellular carcinoma (HCC) cell apoptosis via inducing p65 dephosphorylation at Ser536 and inhibition of NF-κB. Here, we showed that isolie promoted p65/PP2A interaction in vitro and in vivo. Repression of PP2A activity or knockdown of the expression of PP2A-C (the catalytic subunit of PP2A) abrogated isolie-provoked p65 dephosphorylation. I2PP2A is an endogenous PP2A inhibitor. Isolie directly impaired PP2A/I2PP2A interaction. Knockdown of I2PP2A boosted p65/PP2A association and p65 dephosphorylation. Overexpression of I2PP2A restrained isolie-induced p65 dephosphorylation. Untransformed hepatocytes were insensitive to isolie-induced NF-κB inhibition and cell apoptosis. In these cells, basal levels of I2PP2A and p65 phosphorylation at Ser536 were lower than in HCC cells. These findings collectively indicated that isolie suppresses NF-κB in HCC cells through impairing PP2A/I2PP2A interaction and stimulating PP2A-dependent p65 dephosphorylation at Ser536.
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