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LncRNA-p21调控Notch信号通路对非小细胞肺癌A549细胞增殖、迁移及侵袭的影响
引用本文:张冠磊,马苗苗,兰文静,王琳. LncRNA-p21调控Notch信号通路对非小细胞肺癌A549细胞增殖、迁移及侵袭的影响[J]. 肿瘤防治研究, 2021, 48(2): 121-126. DOI: 10.3971/j.issn.1000-8578.2021.20.0730
作者姓名:张冠磊  马苗苗  兰文静  王琳
作者单位:1. 471000 洛阳,河南科技大学第二附属医院呼吸与危重症医学科;2. 450000 郑州,郑州大学第一附属医院肿瘤科
基金项目:河南省高等学校重点科研项目(18A310010)
摘    要:目的 探讨LncRNA-p21调控Notch信号通路对非小细胞肺癌A549细胞增殖、迁移及侵袭的影响。方法 pcDNA-lincRNA-p21、空载质粒pcDNA转染A549细胞设为过表达组和空载组;稳定转染过表达组加入Notch信号通路特异性激活剂Jagged1蛋白,设为Notch激活剂组;不作处理细胞为对照组。MTT法、划痕实验和Transwell小室实验检测各组细胞增殖、迁移和侵袭情况。RT-qPCR及Western blot法检测各组Notch1、HES-1、NICD、E-cadherin、Vimentin的mRNA和蛋白表达。结果 过表达组培养24、48和72 h MTT实验A值均低于对照组、空载组和Notch激活剂组,Notch激活剂组低于对照组和空载组(P<0.05);过表达组48 h细胞迁移率和穿膜细胞数及Notch1、HES-1、NICD、Vimentin mRNA和蛋白相对表达量均低于对照组、空载组和Notch激活剂组,Notch激活剂组低于对照组和空载组(P<0.05);过表达组E-cadherin mRNA和蛋白相对表达量高于对照组和Notch激活剂组,Notch激活剂组高于空载组和对照组(P<0.05)。结论 LncRNA-p21基因过表达可抑制非小细胞肺癌A549细胞增殖、迁移及侵袭,其调控机制可能与抑制Notch信号通路、阻断A549细胞上皮间质转化有关。

关 键 词:非小细胞肺癌  长链非编码RNA-p21  增殖  迁移  侵袭  
收稿时间:2020-06-28

Effect of LncRNA-p21 Regulating Notch Signaling Pathway on Proliferation,Migrationand Invasion of Non-small Cell Lung Cancer A549 Cells
ZHANG Guanlei,MA Miaomiao,LAN Wenjing,WANG Lin. Effect of LncRNA-p21 Regulating Notch Signaling Pathway on Proliferation,Migrationand Invasion of Non-small Cell Lung Cancer A549 Cells[J]. Cancer Research on Prevention and Treatment, 2021, 48(2): 121-126. DOI: 10.3971/j.issn.1000-8578.2021.20.0730
Authors:ZHANG Guanlei  MA Miaomiao  LAN Wenjing  WANG Lin
Affiliation:1. Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of He’nan University of Science and Technology, Luoyang 471000, China; 2. Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450000, China
Abstract:Objective To investigate the effect of LncRNA-p21 on the proliferation, migration and invasion of non-small cell lung cancer A549 cells by regulating Notch signaling pathway. Methods The pcDNAlincRNA-p21 and empty plasmid pcDNA were transfected into A549 cells, and they were divided into overexpression group and empty vector group. Cells from the stably-transfected overexpression group were added with the Notch signaling pathway specific activator Jagged1 protein and set as the Notch activator group. In addition, the cells without treatment were taken as the control group. Cell proliferation, migration and invasion of each group were detected by MTT method, scratch test and Transwell cell test. The expressions of Notch 1, HES-1, NICD, E-cadherin, Vimentin mRNA and protein were detected by RT-qPCR and Western blot. Results The A value of MTT test at 24, 48 and 72 hours in the overexpression group was lower than those in the control group, empty vector group and Notch activator group, and the Notch activator group was higher than the control group and the empty vector group (P<0.05). The cell migration rate, the number of transmembrane cells and the relative expressions of Notch1, HES-1, NICD, Vimentin mRNA and protein of overexpression group at 48 hours were lower than those of the control group, empty vector group and Notch activator group, and the Notch activator group was lower than the control group and the empty vector group (P<0.05). The relative expressions of E-cadherin mRNA and protein of overexpression group were higher than those of control group, empty vector group and Notch activator group, and the Notch activator group was higher than the control group and the empty vector group (P<0.05). Conclusion Overexpression of LncRNA-p21 gene could inhibit the proliferation, migration and invasion of non-small cell lung cancer A549 cells. Its regulatory mechanism may be related to inhibiting Notch signaling pathway, thereby blocking the epithelial-mesenchymal transition of A549 cells.
Keywords:Non-small cell lung cancer  Long non-coding RNA-p21  Proliferation  Migration  Invasion  
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