The type IV phosphodiestera inhibitor rolipram induces expression of the cell cycle inhibitors p21(Cip1) and p27(Kip1), resulting in growth
inhibition, incread differentiation, and subquent apoptosis of malignant A-172 glioma
cells.老诚
期刊名称： Cancer Biology & Therapy
山茶花是什么颜色
中医五脏六腑作者： Chen, Thomas C., Wadsten, Pia, Su, Susan, Rawlinson, Neal, Hofman,
Florence M., Hill, Colin K., Schonthal, Axel H.
年份： 2002年
高清桌面图片鸽子肉怎么做好吃期号： 第3期
我的拉布拉多关键词： Tumor Cells, Cultured;Humans;Glioma;Neoplasm
Invasiveness;Rolipram;Cyclic AMP-Dependent Protein Kinas;Cyclins;Cell Cycle Proteins;Tumor Suppressor Proteins;DNA, Neoplasm
南阳汉画馆
摘要：Upregulation of the cAMP/protein kina A (PKA) pathway has been shown to result in decread proliferation, incread differentiation, and subquent apoptosis of malignant glioma cells. Conventional cAMP analogs, however, are difficult to u in a clinical tting. Therefore, we investigated the effects of rolipram, a drug that has undergone clinical trials as an antidepressant and has also been propod as a treatment for multiple sclerosis. Rolipram acts as a specific inhibitor of type IV phosphodiestera (PDE4), leading to incread intracellular levels of cAMP. We report that the inhibition of PDE4 by rolipram results in the activation of the cAMP/PKA pathway, with potent stimulation of a reporter gene containing a cAMP-responsive element in its promoter region. Further, treatment of the human glioma cell line A-172
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