miR-23a靶向NID2通过Notch通路调控肺癌细胞的侵袭和迁移

发布时间：2018-04-21 04:28

本文选题：miR-a + 肺癌　；参考：《肿瘤防治研究》2017年06期

【摘要】：目的探讨mi R-23a靶向调控NID2蛋白的表达通过Notch通路对肺癌细胞的生物学行为的影响及其机制。方法免疫组织化学检测NID2在肺癌和癌旁正常肺组织中的表达;Western blot检测不同肺癌细胞株中NID2的表达;荧光素酶报告基因检测mi R-23a与NID2的相互作用;Transwell侵袭和划痕实验检测mi R-23a的表达对肺癌细胞侵袭和迁移能力的影响;Western blot检测过表达mi R-23a后肺癌H1650细胞中hes1和NICD蛋白的表达。结果与癌旁正常肺组织相比,肺癌组织中NID2表达明显增高;H1650肺癌细胞株中NID2的表达水平最高;在肺癌H1650细胞中,mi R-23a能与NID2的3’UTR特异性结合,调控NID2的表达;mi R-23a可调控肺癌H1650细胞的侵袭迁移能力;过表达mi R-23a可以抑制肺癌H1650细胞中hes1和NICD的表达。结论 mi R-23a可以靶向NID2通过Notch信号通路调控肺癌细胞的侵袭和迁移。
[Abstract]:Objective to investigate the effect of mi R-23a targeted regulation of NID2 protein expression on the biological behavior of lung cancer cells through Notch pathway and its mechanism. Methods the expression of NID2 in lung cancer and adjacent normal lung tissues was detected by immunohistochemistry. The expression of NID2 in different lung cancer cell lines was detected by Western blot. Luciferase reporter gene was used to detect the interaction between mi R-23a and NID2. The effect of the expression of mi R-23a on the invasion and migration of lung cancer cells was detected by Transwell invasion and scratch assay. The expression of hes1 and NICD in H1650 cells was detected by Western blot after overexpression of mi R-23a. Results the expression of NID2 in lung cancer tissues was significantly higher than that in adjacent normal lung tissues. The expression of NID2 in H1650 lung cancer cell line was the highest, and the expression of miR-23a could specifically bind to the 3'UTR of NID2 in H1650 cells. The overexpression of miR-23a could inhibit the expression of hes1 and NICD in H1650 cells, while the overexpression of miR-23a could inhibit the invasion and migration of H1650 cells. Conclusion mi R-23a can target NID2 to regulate the invasion and migration of lung cancer cells through Notch signaling pathway.
【作者单位】：南阳市中心医院肿瘤内科;
【分类号】：R734.2

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