Apoptotic Effects of Cordycepin Through the Extrinsic Pathway and p38 MAPK Activation in Human Glioblastoma U87MG Cells
Apoptotic Effects of Cordycepin Through the Extrinsic Pathway and p38 MAPK Activation in Human Glioblastoma U87MG Cells
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DOI：
10.4014/jmb.1507.07090
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发表时间：
2016-02-01
影响因子：
2.8
通讯作者：
Lee, Young-Choon
中科院分区：
文献类型：
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作者：
Baik, Ji-Sue;Mun, Seo-Won;Lee, Young-Choon
我们首先证明，虫草素抑制细胞生长，并引发细胞凋亡的U87 MG细胞与野生型p53，但不是在T98 G细胞与突变型p53。Western blot结果显示，虫草素处理的U87 MG细胞中，caspase-8、-3和Bcl-2的表达水平下调，而Fas、FasL、巴克、裂解的caspase-3、-8和裂解的PARP的表达水平上调，表明虫草素通过激活死亡受体介导的途径诱导U87 MG细胞凋亡。虫草素诱导的细胞凋亡仅能被p38 MAPK特异性抑制剂SB 203580抑制。这些结果表明，虫草素通过激活p38 MAPK和抑制Akt存活途径引发U87 MG细胞凋亡。
We first demonstrated that cordycepin inhibited cell growth and triggered apoptosis in U87MG cells with wild-type p53, but not in T98G cells with mutant-type p53. Western blot data revealed that the levels of procaspase-8, -3, and Bcl-2 were downregulated in cordycepin-treated U87MG cells, whereas the levels of Fas, FasL, Bak, cleaved caspase-3, -8, and cleaved PARP were upregulated, indicating that cordycepin induces apoptosis by activating the death receptor-mediated pathway in U87MG cells. Cordycepin-induced apoptosis could be suppressed by only SB203580, a p38 MAPK-specific inhibitor. These results suggest that cordycepin triggered apoptosis in U87MG cells through p38 MAPK activation and inhibition of the Akt survival pathway.