| 李 哲,卢 强,陈 晓,张继朋,王武平,范晓东.NOK在雌激素促进肺腺癌细胞系上皮间质转化过程中的作用[J].,2021,(13):2427-2431 |
| NOK在雌激素促进肺腺癌细胞系上皮间质转化过程中的作用 |
| The Role of NOK in the Process of Epithelial Stromal Transformation of Lung Adenocarcinoma Cell Line Promoted by Estrogen |
| 投稿时间：2020-12-28 修订日期：2021-01-23 |
| DOI：10.13241/j.cnki.pmb.2021.13.006 |
| 中文关键词: NOK 肺腺癌 上皮间质转化 |
| 英文关键词: NOK Lung adenocarcinoma Epithelial stromal transformation |
| 基金项目:国家自然科学基金项目（81572252） |
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| 中文摘要: |
| 摘要 目的：探讨NOK（Novel Oncogene with Kinase-domain：蛋白络氨酸激酶结构域新基因）在雌激素促进肺腺癌细胞系上皮间质转化过程中的作用。方法：实验共分四组，其中第一组细胞NOK基因不下调，不加雌激素，为空白对照组，第二组细胞NOK基因下调，不加雌激素，第三组细胞NOK基因不下调，加雌激素，第四组细胞NOK基因下调，加雌激素。用慢病毒下调A549细胞系中NOK基因表达量，并用浓度为1×10-8 mol/L的雌激素刺激各组细胞，用q-RT-PCR及Western blot方法检测各组细胞中NOK和EMT标志物表达量，用Transwell实验检测各组细胞的迁移能力。结果：相比于第一组，第二组细胞中NOK和Vimentin表达量降低、E-cadherin表达量增高，分别为0.09±0.01、0.16±0.02、4.83±0.61，与第一组有统计学差异；第三组细胞中NOK和Vimentin表达量显著增高、E-cadherin表达量显著降低，分别为6.03±0.92、5.77±0.86、0.33±0.04，与第一组有统计学差异；第四组细胞中NOK和Vimentin表达量降低、E-cadherin表达量增高，分别为0.11±0.01、0.19±0.03、4.92±0.59，与第一组有统计学差异，与第二组无统计学差异。各组细胞中NOK和EMT标志物的蛋白表达量与mRNA表达量的趋势一致。第二组细胞迁移数显著低于第一组，组间有统计学差异，第三组细胞迁移数显著高于第一组，组间有统计学差异，第四组细胞迁移数显著低于第一组，组间有统计学差异。结论：雌激素可以促进肺腺癌细胞系EMT过程，而下调NOK基因表达可以阻断这一过程，由此认为，雌激素可以通过NOK调控肺腺癌EMT过程。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the role of NOK in the process of epithelial stromal transformation of lung adenocarcinoma cell line promoted by estrogen. Methods: The experiment was divided into four groups, the NOK gene was not down regulated in the first group without estrogen, the NOK gene was down regulated in the second group without estrogen, the NOK gene was not down regulated in the third group with estrogen, the NOK gene was down regulated in the fourth group with estrogen. The NOK gene in A549 cell line was down regulated by lentivirus, the cells were stimulated by estrogen at a concentration of 1×10-8 mol/L, the expression of NOK and EMT markers in each group were detected by q-RT-PCR and Western blot, and the migration ability of cells in each group was detected by Transwell test. Results: The expression of NOK and Vimentin in the second group decreased and the expression of E-cadherin increased compared with the first group, which were 0.09±0.01, 0.16±0.02 and 4.83±0.61, which were statistically different from the first group. The expression of NOK and Vimentin in the third group increased significantly and the expression of E-cadherin decreased, which were 6.03±0.92, 5.77±0.86 and 0.33±0.04, which were statistically different from the first group. In the fourth group, the expression of NOK and vimentin decreased and the expression of E-cadherin increased, which were 0.11±0.01, 0.19±0.03 and 4.92±0.59, there were statistical differences with the first group and no statistical differences with the second group. The trend of protein expression of NOK and EMT markers was consistent with that of mRNA expression. The number of cell migration in the second group was significantly lower than that in the first group, and there was statistical difference between the two groups. The number of cell migration in the third group was significantly higher than that in the first group, and there was statistical difference between the two groups. The number of cell migration in the fourth group was significantly lower than that in the first group, and there was statistical difference between the two groups. Conclusion: Estrogen can promote the EMT process of lung adenocarcinoma cell lines, and down regulating the expression of NOK gene can block this process. Therefore, estrogen can regulate the EMT process of lung adenocarcinoma through NOK gene. |
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