Hypoglycemia-induced c-Jun phosphorylation is mediated by c-Jun N-terminal kinase 1 and Lyn kinase in drug-resistant human breast carcinoma MCF-7/ADR cells
Hypoglycemia-induced c-Jun phosphorylation is mediated by c-Jun N-terminal kinase 1 and Lyn kinase in drug-resistant human breast carcinoma MCF-7/ADR cells
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DOI：
10.1074/jbc.272.18.11690
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发表时间：
1997-05-02
影响因子：
4.8
通讯作者：
Lee, YJ
中科院分区：
文献类型：
--
作者：
Liu, X;Gupta, AK;Lee, YJ
我们研究了MCF-7/ADR细胞缺糖后c-Jun磷酸化的信号转导机制。缺糖后MCF-7/ADR细胞酪氨酸磷酸化立即增加，并特异性激活src家族酪氨酸激酶林恩激酶。此外，低血糖处理强烈激活c-Jun N-末端激酶1（JNK 1），导致c-Jun磷酸化和激活，林恩反义寡核苷酸实验表明，林恩激酶激活是JNK 1激活的原因，而不是细胞外信号调节激酶。我们还观察到葡萄糖剥夺诱导的MCF-7/ADR细胞中Ras活化。这些结果表明，一个可能的Ras依赖性信号通路涉及林恩激酶和JNK 1，这导致在MCF-7/ADR细胞的葡萄糖剥夺诱导的反应。
We studied the signal transduction mechanism that is involved in c-Jun phosphorylation evident after glucose deprivation in MCF-7/ADR cells, Glucose deprivation caused an immediate increase in tyrosine phosphorylation in MCF-7/ADR cells and specifically activated Lyn kinase, a src family tyrosine kinase. In addition, hypoglycemic treatment strongly activated c-Jun N-terminal kinase 1 (JNK1), leading to the phosphorylation and activation of c-Jun. Experiments with Lyn antisense oligonucleotides demonstrated that Lyn kinase activation was responsible for the activation of JNK1 but not extracellular signal-regulated kinase. We also observed glucose deprivation-induced Ras activation in MCF-7/ADR cells. These results indicate a possible Ras-dependent signaling pathway involving Lyn kinase and JNK1, which leads to the glucose deprivation-induced responses in MCF-7/ADR cells.