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首页> 外文期刊>The British Journal of Nutrition >Mitogen-activated protein kinase mediates the apoptosis of highly metastatic human non-small cell lung cancer cells induced by isothiocyanates.
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Mitogen-activated protein kinase mediates the apoptosis of highly metastatic human non-small cell lung cancer cells induced by isothiocyanates.

机译：丝裂原活化的蛋白激酶介导异硫氰酸盐诱导的高转移性人非小细胞肺癌细胞的凋亡。

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Dietary isothiocyanates have been shown to possess anti-tumour activity, inhibiting several types of cultured human cancer cell growth. However, there are limited studies on their effects on cancer cell metastasis. Our previous study showed that benzyl isothiocyanate (BITC) and phenethyl isothiocyanate (PEITC) suppressed human lung cancer cell metastasis potential. In the present study, we found BITC (7.5 and 10 muM) and PEITC (12.5 and 20 muM) induced highly metastatic human non-small cell lung cancer L9981 cell apoptosis in a dose-dependent manner. Caspase-3 was activated. They also caused cell cycle arrest at the G2/M phase, via modulation of cyclin B1 expression. The mitogen-activated protein kinase (MAPK) signalling pathway was involved. c-Jun N-terminal kinase, extracellular signal-regulated protein kinase 1/2 and p38 were activated in a dose-dependent manner; activator protein 1 (AP-1) transcriptional activation and cyclin D1 expression were repressed. Apoptosis and MAPK activation were abrogated by anti-oxidant N-acetyl cysteine (NAC), suggesting that cell death signalling was triggered by oxidative stress. Further microarray analysis evaluated the potential targeted genes related to apoptosis and the cell cycle. Our studies suggested that BITC and PEITC suppressed the metastasis potential of highly metastatic lung cancer cells by inducing apoptosis and cell cycle arrest, via targeting the MAPK/AP-1 pathway. This may provide a novel approach for metastasis therapy of lung cancer by dietary isothiocyanates and possibly other types of cancer
机译：膳食异硫氰酸盐已显示具有抗肿瘤活性，可抑制几种培养的人类癌细胞的生长。然而，关于它们对癌细胞转移的影响的研究很少。我们以前的研究表明，异硫氰酸苄酯（BITC）和异硫氰酸苯乙酯（PEITC）抑制人肺癌细胞的转移潜力。在本研究中，我们发现BITC（7.5和10μM）和PEITC（12.5和20μM）以剂量依赖的方式诱导高度转移的人非小细胞肺癌L9981细胞凋亡。 Caspase-3被激活。它们还通过调节细胞周期蛋白B1的表达，使细胞周期停滞在G 2 / M期。有丝分裂原激活的蛋白激酶（MAPK）信号传导途径。 c-Jun N-末端激酶，细胞外信号调节蛋白激酶1/2和p38以剂量依赖性方式被激活。激活蛋白1（AP-1）转录激活和细胞周期蛋白D1表达被抑制。抗氧化剂 N -乙酰半胱氨酸（NAC）消除了细胞凋亡和MAPK活化，表明细胞死亡信号是由氧化应激触发的。进一步的微阵列分析评估了与凋亡和细胞周期有关的潜在靶向基因。我们的研究表明，BITC和PEITC通过靶向MAPK / AP-1途径诱导凋亡和细胞周期停滞，从而抑制了高度转移性肺癌细胞的转移潜力。这可能为饮食中异硫氰酸盐和其他类型癌症的肺癌转移治疗提供一种新方法

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