Notch1 induces enhanced expression of Δ-like-1 in the U251MG glioma cell line
Notch1 induces enhanced expression of Δ-like-1 in the U251MG glioma cell line
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DOI：
10.3892/ijmm_00000251
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发表时间：
2009-10
影响因子：
5.4
通讯作者：
Chunfa Qian;Wei Yan;Junxia Zhang;Lei Shi;Jinfeng Qian;Zhen Fu;C. Kang;Ning Liu;Y. You
中科院分区：
文献类型：
--
作者：
Chunfa Qian;Wei Yan;Junxia Zhang;Lei Shi;Jinfeng Qian;Zhen Fu;C. Kang;Ning Liu;Y. You
Notch信号通路参与细胞生长、存活和分化的协调调节。先前的研究结果表明，Notch 1和Delta-like-1（DLL 1）在许多胶质瘤细胞系和原发性人脑胶质瘤中过表达。通过RNA干扰下调DLL 1在多种胶质瘤细胞系中抑制增殖并诱导凋亡我们的研究表明，Notch 1表达质粒在U251 MG胶质瘤细胞系中诱导DLL 1的表达增加。粘附，阻断Notch 1受体下调DLL 1的表达。下调DLL 1和阻断Notch 1受体均能诱导U251 MG细胞凋亡和增殖抑制，两种方法联合应用的作用强于单一方法。这些发现表明Notch 1和DLL 1之间存在正反馈回路，可能成为有效的联合治疗靶点。
The Notch signaling pathway takes part in coordinated regulation of cell growth, survival and differentiation. Previous findings have shown that Notch1 and Delta-like-1 (DLL1) are overexpressed in many glioma cell lines and primary human gliomas. Down-regulation of DLL1 by RNA interference inhibits proliferation and induces apoptosis in multiple glioma cell lines. Our studies showed that Notch1 expression plasmid induced more expression of DLL1 in the U251MG glioma cell line. Adversely, blocking Notch1 receptors down-regulated the expression of DLL1. Both down-regulating DLL1 and blocking Notch1 receptors induced U251MG cell apoptosis and proliferation inhibition, and combining the two treatments produced stronger effects than the sum of a single treatment. These findings suggest a positive feedback loop between Notch1 and DLL1, which may become an effective combined therapeutic target.