Hung Huey-Shan, Wu Wen-Jun, Cheng Ya-Wen, Wu Ming-Fan, Chang Kee-Lung, Lee Huei
Institite of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, ROC.
J Toxicol Environ Health A. 2005 Sep;68(17-18):1525-35. doi: 10.1080/15287390590967487.
Cooking oil fumes (COF) exposure was demonstrated to be associated with lung cancer development in Taiwanese nonsmoking women. Previous studies identified Cox-2 overexpression and oxidative DNA damage in lung adenocarcinoma cells after exposure to COF. Involvement of COF in lung tumorigenesis may be associated with cell survival, as well as proliferation of lung adenocarcinoma. To test this hypothesis, A549, a lung adenocarcinoma cell line, was used, and MTT assay data showed that the cell viability of A549 was significantly increased in a concentration-dependent manner by COF treatment for 48 h. Flow cytometery results indicated that the proportion of A549 cell at S-phase was markedly increased after exposure of COF. To elucidate whether the anti-apoptotic c-IAP2 (IAP2) was involved in COF-improved cell survival, IAP2 protein levels was determined by Western blot, and the results showed it was significantly induced by COF in a concentration-dependent manner. Moreover, the suppression of BAY, a nuclear factor (NF)-kappaB binding inhibitor, or the COF-induced IAP2 protein levels indicated that NF-kappaB activation by COF may partly be involved in IAP2 induction. These results showed that the positive impact of COF on cell survival and proliferation of A549 lung tumor cells may be through an induction of IAP2 overexpression.
在台湾非吸烟女性中，食用油油烟（COF）暴露被证明与肺癌发生有关。先前的研究发现，暴露于COF后，肺腺癌细胞中Cox-2过表达和氧化性DNA损伤。COF参与肺肿瘤发生可能与细胞存活以及肺腺癌增殖有关。为了验证这一假设，使用了肺腺癌细胞系A549，MTT分析数据显示，COF处理48小时后，A549细胞活力以浓度依赖性方式显著增加。流式细胞术结果表明，暴露于COF后，A549细胞处于S期的比例显著增加。为了阐明抗凋亡蛋白c-IAP2（IAP2）是否参与COF改善的细胞存活，通过蛋白质免疫印迹法测定IAP2蛋白水平，结果显示其在COF作用下呈浓度依赖性显著诱导。此外，核因子（NF）-κB结合抑制剂BAY的抑制或COF诱导的IAP2蛋白水平表明，COF激活NF-κB可能部分参与IAP2的诱导。这些结果表明，COF对A549肺肿瘤细胞存活和增殖的积极影响可能是通过诱导IAP2过表达实现的。
