机构地区:[1]河南省胸科医院,450000
出 处:《实用癌症杂志》2022年第1期16-21,共6页The Practical Journal of Cancer
基 金:河南省科技攻关项目(编号:202102310036)。
摘 要:目的探讨miR-181c-5p调控非小细胞肺癌细胞A549的潜在机制。方法检测非小细胞肺癌细胞A549和人正常肺细胞HLF-a中miR-181c-5p的表达水平。过表达或敲低miR-181c-5p后,检测非小细胞肺癌细胞A549的凋亡水平。通过miRDB在线分析miR-181c-5p潜在底物,过表达miR-181c-5p后,通过实时荧光定量PCR检测潜在底物的表达水平。敲低潜在底物后,检测非小细胞肺癌细胞A549的凋亡水平。结果miR-181c-5p在非小细胞肺癌细胞A549中的表达水平低于人正常肺细胞HLF-a(P<0.05)。过表达miR-181c-5p后,非小细胞肺癌细胞A549的凋亡上升(P<0.05);敲低miR-181c-5p后,非小细胞肺癌细胞A549的凋亡下降(P<0.05)。敲低TRIM71时,非小细胞肺癌细胞A549的凋亡水平上升(P<0.05)。过表达TRIM71后,非小细胞肺癌细胞A549的凋亡水平下降(P<0.05)。过表达miR-181c-5p后,TRIM71的蛋白水平下降;而敲低miR-181c-5p后,TRIM71的蛋白水平上升。敲低TRIM71后,非小细胞肺癌细胞A549的P53水平上升;而过表达TRIM71后,非小细胞肺癌细胞A549的p53水平下降。过表达miR-181c-5p后,非小细胞肺癌细胞A549的p53水平上升;而敲低miR-181c-5p后,非小细胞肺癌细胞A549的p53水平下降。结论miR-181c-5p通过靶向TRIM71 mRNA的3端非编码区后降低了TRIM71的表达水平,随后凋亡活化基因p53的蛋白水平上升,最后促进了非小细胞肺癌细胞A549的凋亡。Objective To explore the potential mechanism of miR-181c-5p in regulating non-small cell lung cancer cell A549.Methods To detect the expression level of miR-181c-5p in non-small cell lung cancer cell A549 and human normal lung cell HLF-a.After overexpression or knockdown of miR-181c-5p,the apoptosis level of non-small cell lung cancer cell A549 was detected.The potential substrates of miR-181c-5p were analyzed online by miRDB.After miR-181c-5p was overexpressed,the expression level of potential substrates was detected by real-time fluorescent quantitative PCR.After knocking down the potential substrate,the apoptosis level of non-small cell lung cancer cell A549 was detected.Results The expression level of miR-181c-5p in non-small cell lung cancer cell A549 was lower than that of human normal lung cell HLF-a(P<0.05).After overexpression of miR-181c-5p,the apoptosis of non-small cell lung cancer cell A549 increased(P<0.05);after knocking down miR-181c-5p,the apoptosis of non-small cell lung cancer cell A549 decreased(P<0.05).When TRIM71 was knocked down,the apoptosis level of non-small cell lung cancer cell A549 increased(P<0.05).After overexpression of TRIM71,the apoptotic level of non-small cell lung cancer cell A549 decreased(P<0.05).After overexpression of miR-181c-5p,the protein level of TRIM71 decreased;after knocking down miR-181c-5p,the protein level of TRIM71 increased.After knocking down TRIM71,the p53 level of non-small cell lung cancer cell A549 increased;and after overexpression of TRIM71,the p53 level of non-small cell lung cancer cell A549 decreased.After overexpression of miR-181c-5p,the p53 level of non-small cell lung cancer cell A549 increased;and after knocking down miR-181c-5p,the p53 level of non-small cell lung cancer cell A549 decreased.Conclusion miR-181c-5p reduces the expression level of TRIM71 by targeting the 3 terminal non-coding region of TRIM71 mRNA,and then increases the protein level of the apoptosis-activating gene p53,and finally promotes the apoptosis of non-small cell lung canc
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