Dual blockade of mitogen-activated protein kinases ERK-1 (p42) and ERK-2 (p44) and cyclic AMP response element binding protein (CREB) by neomycin inhibits glioma cell proliferation
Dual blockade of mitogen-activated protein kinases ERK-1 (p42) and ERK-2 (p44) and cyclic AMP response element binding protein (CREB) by neomycin inhibits glioma cell proliferation
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DOI：
10.1179/016164103101201030
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发表时间：
2003-01-01
影响因子：
1.9
通讯作者：
Dujovny, M
中科院分区：
文献类型：
--
作者：
Cuevas, P;Diaz-González, D;Dujovny, M
几种生长因子及其受体在神经胶质瘤中以不适当的高丰度表达，并且在从低度恶性到高度恶性的转变过程中进一步上调。在神经胶质瘤细胞中，生长因子诱导丝裂原活化蛋白激酶（MAPK）途径的表达。在这里，我们报告，新霉素抑制胶质瘤细胞增殖在体外抑制p42/44 MAPK和环AMP元件结合蛋白（CREB）指导的转录途径。由于通过抑制特异性转录调节蛋白来改变基因转录具有重要的治疗潜力，新霉素为治疗癌症和与持续MAPK活性相关的其他疾病提供了巨大的希望[Neurol Res 2003; 25：13-16]。
Several growth factors and their receptors are expressed in inappropriately high abundance in gliomas and are further upregulated during the transition from low- to high-grade malignancy. In glioma cells growth factors induce expression of mitogen-activated protein kinase (MAPK) pathways. Here we report that neomycin restrained glioma cell proliferation in vitro by inhibition of p42/44 MAPK and the cyclic AMP element binding protein (CREB)-directed transcription pathways. Since alteration of gene transcription by inhibition of specific transcriptional regulatory proteins has important therapeutic potential, neomycin offers great promise for treating cancer and other diseases associated with a sustained MAPK activity [Neurol Res 2003; 25: 13-16].