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Title of article :
Oridonin induces G2/M arrest and apoptosis via activating ERK–p53 apoptotic pathway and inhibiting PTK–Ras–Raf–JNK survival pathway in murine fibrosarcoma L929 cells
Author/Authors :
Cheng، نويسنده , , Yan-Xuan Qiu، نويسنده , , Feng and Ye، نويسنده , , Yuan-chao and Tashiro، نويسنده , , Shin-ichi and Onodera، نويسنده , , Satoshi and Ikejima، نويسنده , , Takashi، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2009
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Abstract :
Oridonin was reported to induce L929 cell apoptosis via ROS-mediated mitochondrial and ERK pathways; however, the precise mechanisms by which oridonin induces cell death remain unclear. Herein, we found that oridonin treatment induced an increase in G2/M phase cell percentage. And, G2/M phase arrest was associated with down-regulation of cell cycle related cdc2, cdc25c and cyclinB levels, as well as up-regulation of p21 and p-cdc2 levels. In addition, we discovered that interruption of p53 activation decreased oridonin-induced apoptosis, and blocking ERK by specific inhibitors or siRNA suppressed oridonin-induced p53 activation. Moreover, inhibition of PTK, protein kinase C, Ras, Raf or JNK activation increased oridonin-induced apoptosis. Also, the level of Ras, Raf or JNK was down-regulated by oridonin, and the inhibition of PTK, Ras, Raf activation decreased p-JNK level. In conclusion, oridonin induces L929 cell G2/M arrest and apoptosis, which is regulated by promoting ERK–p53 apoptotic pathway and suppressing PTK-mediated survival pathway.
Keywords :
p53 , Protein tyrosine kinase (PTK) , Oridonin , G2/M phase arrest , apoptosis
Journal title :
Archives of Biochemistry and Biophysics
Journal title :
Archives of Biochemistry and Biophysics
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