| Wentilactone A抑制小细胞肺癌系NCI-H1688细胞的迁移研究 |
| 投稿时间：2016-01-27 修订日期：2016-03-31 点此下载全文 |
| 引用本文：姜文丽,黄才国.Wentilactone A抑制小细胞肺癌系NCI-H1688细胞的迁移研究[J].药学实践杂志,2016,34(3):219~222,274 |
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| 基金项目:国家自然科学基金面上项目(41576160,81473239) |
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| 中文摘要:目的 探讨小分子化合物Wentilactone A (WA)抑制小细胞肺癌(small cell lung cancer,SCLC)细胞系NCI-H1688细胞迁移的机制。方法 采用划痕实验、噻唑蓝[3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide,MTT]实验检测小分子化合物WA对细胞迁移和增殖能力的影响。免疫荧光实验检测化合物WA作用后SCLC细胞系NCI-H1688细胞中ATF3蛋白的表达。Western blot验证ATF3/Nrf2/AKR1C1信号通路的关键蛋白。结果 小分子化合物WA抑制SCLC细胞系NCI-H1688细胞的迁移和增殖,加入化合物WA 24 h组与48 h组的IC50分别为(1.03±0.30)和(0.46±0.18) μmol/L。WA作用组NCI-H1688细胞的相对迁移距离为(8.73±1.06) mm,低于对照组的(15.63±3.11) mm,过表达AKR1C1基因后NCI-H1688细胞迁移距离为(24.37±0.90) mm,过表达AKR1C1基因并且WA作用后NCI-H1688细胞的迁移距离为(14.17±1.31) mm,差异有统计学意义(P<0.05)。ATF3是AKR1C1基因的负性调节因子,化合物WA作用后,ATF3蛋白表达水平升高,抑制Nrf2与ARE结合,从而抑制AKR1C1蛋白的表达。结论 WA通过ATF3/Nrf2/AKR1C1信号通路抑制SCLC细胞系NCI-H1688细胞的迁移和增殖。 |
| 中文关键词:Wentilactone A 小细胞肺癌 迁移 增殖 |
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| Wentilactone A inhibition of migration of small cell lung carcinoma NCI-H1688 cell line |
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| Abstract:Objective To investigate mechanism of Wentilactone A (WA) inhibition of small cell lung cancer(SCLC) cell line NCI-H1688 migration. Methods The migration and proliferation were analyzed by wounding-healing assay and MTT assay[3- (4, 5-Dimethylthiazol-2-yl) -2, 5-diphenyltetrazolium bromide, MTT]. Immunofluorescence was used to confirm the expression of ATF3 protein after WA treatment. Western blot was used to examine the expression of key proteins in ATF3/Nrf2/AKR1C1 signal pathway. Results WA inhibits the proliferation and migration of SCLC. MTT analysis showed WA inhibits the proliferation of NCI-H1688 cell line in a time-dependent manner. The number of migrated cells in WA treatment group was (8.73±1.06) mm, which was lower than that of control group (15.63±3.11) mm, The number of migrated cells in AKR1C1 expression group was (24.37±0.90) mm, the number of migrated cells in AKR1C1 expression and WA treatment group was (14.17±1.31) mm, with significant difference (P<0.05). WA enhances the nuclear expression of ATF3, and then reduces the expression of p-Nrf2 and AKR1C1. Conclusion WA inhibits the proliferation and migration of SCLC through ATF3/Nrf2/AKR1C1 signal pathway. |
| keywords:Wentilactone A SCLC migration proliferation |
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