| 饶钟鸣,马慧,关耀武.微 RNA?21调控的蛋白酪氨酸磷酸酶 MEG2蛋白低表达促进肺癌发生发展的分子机制[J].安徽医药,2020,24(7):1434-1439. |
| 微 RNA?21调控的蛋白酪氨酸磷酸酶 MEG2蛋白低表达促进肺癌发生发展的分子机制 |
| Molecular mechanism of low expression of protein tyrosine phosphatase MEG2 protein regulated by miR?21 to promote lung carcinoma develpoment |
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| DOI：10.3969/j.issn.1009?6469.2020.07.042 |
| 中文关键词: 肺肿瘤/病因学 蛋白酪氨酸磷酸酶，非受体 2型 微 RNA?21 增殖 侵袭 凋亡 |
| 英文关键词: Lung neoplasms/etiology Protein tyrosine phosphatase,non-receptor type 2 miR?21 Proliferation Invasion Apoptosis |
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| 中文摘要: |
| 目的蛋白酪氨酸磷酸酶 MEG2蛋白在肺癌中异常低表达及促进肺癌发生发展的分子机制。方法预测靶向 MEG2的 miRNAs；分别运用蛋白质印迹法( Western blot)和 qRT?PCR检测肺癌组织的 MEG2蛋白、 mRNA和 miR?21表达水平；将肺癌细胞分为四组，分别为过表达对照组、 miR?21过表达组、抑制对照组及 miR?21抑制组，在肺癌细胞中通过转染 miR?21前体或反义 miR?21以过表达或敲降 miR?21以及利用荧光素酶报告方法检测 miR?21对 MEG2是否直接靶向。分别利用 CCK?8、Tran? swell和细胞凋亡试剂盒检测 miR?21通过调控 MEG2对肺癌细胞增殖、侵袭以及凋亡的作用。结果预测发现 miR?21在 MEG2 3’UTR上有直接结合位点。蛋白质印迹法和 qRT?PCR结果显示肺癌组织 MEG2和 miR?21呈负相关。过表达或敲降 miR?21实验显示 MEG2是 miR?21的直接靶基因(过表达组变化倍数: A549 0.26，H1975 0.18；敲降组变化倍数: A549 2.48， H1975 2.18)。体外实验显示 miR?21抑制 MEG2的表达从而促进增殖(对照 3.35，miR?21过表达 4.78)以及抑制凋亡(对照 5.68，miR?21过表达 3.28)。结论 miR?21?MEG2形成的新调控轴直接参与调节肺癌的增殖、侵袭和凋亡。 |
| 英文摘要: |
| Objective To investigate The abnormally low expression of MEG2 protein in lung cancer and the molecular mechanismof promoting the development of lung cancer.Methods Bioinformatics were performed to predict the miRNAs targeting MEG2.Western blot and qRT?PCR were employed to analysis MEG2 protein，mRNA expression and miR?21 in lung cancer tissues.Lung cancer cells were divided into four groups，miR?NC，miR?21，anti?miR?NC and anti?miR?21 group，respectively，the direct correla? tion between miR?21 and MEG2 was monitored via overexpression or knockdown of miR?21 and luciferase reporter assay in lungcancer cells.The effects of miR?21?targeted MEG2 on proliferation，invasion and apoptosis of lung cancer cells were tested by CCK? 8 assay，transwell assay and cell apoptosis kit.The impact of miR?21?targeted MEG2 on the growth of lung tumor was detected by CCK?8，Transwell and apoptosis kit.Results Bioinformatics prediction showed that miR?21 specifically bounded to MEG2 3 'UTR. As expected，a negative correlation between MEG2 and miR?21 in lung cancer tissues was found via Western blot and qRT?PCR as?says. We further experimentally validated MEG2 as a direct target of miR?21 by evaluating MEG2 expression in lung cancer cellsafter the overexpression or knockdown of miR?21 and by luciferase assay(Fold change in overexpression group:A549 0.26，H1975 |
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