Inhibitory Effects of Scutellarein on Proliferation of Human Lung Cancer A549 Cells through ERK and NFκB Mediated by the EGFR Pathway
Inhibitory Effects of Scutellarein on Proliferation of Human Lung Cancer A549 Cells through ERK and NFκB Mediated by the EGFR Pathway
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DOI：
10.4077/cjp.2014.bac200
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发表时间：
2014-08-31
影响因子：
1.8
通讯作者：
Kao, Erl-Shyh
中科院分区：
文献类型：
--
作者：
Cheng, Chun-Yuan;Hu, Chao-Chin;Kao, Erl-Shyh
高表达的环氧合酶-2（考克斯-2）对人肺癌细胞具有较强的增殖能力，其作用与表皮生长因子受体（EGFR）通路有关，而EGFR通路由细胞外信号调节激酶（ERK）和核因子κ B（NF kappa B）介导。在这项研究中，黄芩素，黄酮类化合物，筛选在不同浓度（0，5，25和50 μ M）在24小时或48小时在人肺癌细胞系A549的增殖抑制。结果表明，50 μ M黄芩素作用A549细胞24 h和48 h后，细胞增殖受到抑制。不同浓度的野黄芩素处理24 h后，磷酸化EGFR、磷酸化ERK、磷酸化NF kappa B和考克斯-2的表达水平均呈剂量依赖性降低。此外，ERK抑制剂U 0126和NF κ B抑制剂MG 132也抑制A549细胞增殖，与50 μ M黄芩素处理24 h至48 h相似。实验结果表明，灯盏乙素可通过EGFR途径介导的ERK和NF-κ B抑制人肺癌A549细胞的增殖。
High expression levels of cyclooxygenase-2 (COX-2) contribute a strong proliferative ability to human lung cancer cells, and this function is link to the epidermal growth factor receptor (EGFR) pathway, which was mediated by extracellular-signal-regulated kinase (ERK) and nuclear factor kappa B (NF kappa B). In this study, scutellarein, a flavonoid compound, was screened for proliferation inhibition at different concentrations (0, 5, 25 and 50 mu M) at 24 h or 48 h in human lung cancer cell line A549. Results showed that A549 cell proliferation was inhibited by 50 mu M scutellarein treatment in 24 h and 48 h of treatment. The expression levels of phosphorylated EGFR, phosphorylated ERK, phosphorylated NF kappa B and COX-2 were reduced in a dose-dependent manner after 24 h scutellarein treatments at different concentrations. Further, ERK inhibitor U0126 and NF kappa B inhibitor MG132 also inhibited A549 cell proliferation similar to 50 mu M scutellarein treatment from 24 h to 48 h. The experimental results showed that scutellarein could inhibit proliferation of the human lung cancer cell line A549 through ERK and NF-kappa B mediated by the EGFR pathway.