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lncRNA ADPGK-AS1通过调控miR-217表达对非小细胞肺癌细胞增殖和凋亡的影响
引用本文:肖钦晓,程宏宁,颜洪顺,王春刚,陆小珠. lncRNA ADPGK-AS1通过调控miR-217表达对非小细胞肺癌细胞增殖和凋亡的影响[J]. 临床肺科杂志, 2020, 25(7): 998-1004
作者姓名:肖钦晓  程宏宁  颜洪顺  王春刚  陆小珠
作者单位:571400 海南 琼海,琼海市人民医院呼吸内科;570311 海南 海口,海南省人民医院呼吸内科
摘    要:目的研究lncRNA ADPGK-AS1和miR-217在非小细胞肺癌中的表达及其对非小细胞肺癌A549细胞增殖和凋亡的影响。方法以癌旁组织为对照,qRT-PCR检测lncRNA ADPGK-AS1和miR-217在116例非小细胞肺癌组织中的表达水平,双荧光素酶报告系统验证ADPGK-AS1和miR-217的调控关系,在A549细胞中转染si-ADPGK-AS1和miR-217以抑制lncRNA ADPGK-AS1和过表达miR-217,MTT法和流式细胞术检测A549细胞增殖和凋亡,Western blot检测细胞中CyclinD1、p21、Bax和Bcl-2的蛋白表达水平。结果与癌旁组织相比,在116例非小细胞肺癌组织中lncRNA ADPGK-AS1的含量显著升高(P<0.05),miR-217的含量则显著下降(P<0.05);lncRNA ADPGK-AS1靶向负调控miR-217的表达;抑制ADPGK-AS1表达和过表达miR-217均可抑制非小细胞肺癌A549细胞增殖并促进细胞凋亡,使细胞中CyclinD1和Bcl-2含量降低(P<0.05),p21和Bax含量升高(P<0.05);干扰miR-217表达逆转了抑制ADPGK-AS1表达对A549细胞增殖、凋亡的作用。结论 LncRNA ADPGK-AS1可能通过靶向miR-217促进非小细胞肺癌A549细胞增殖,抑制细胞凋亡。LncRNA ADPGK-AS1可能是非小细胞肺癌的潜在分子靶点。

关 键 词:非小细胞肺癌  A549细胞  ADPGK-AS1  miR-217  增殖  凋亡

Effect of lncRNA ADPGK-AS1 on proliferation and apoptosis of non-small cell lung cancer cells by regulating the expression of miR-217
XIAO Qin-xiao,CHENG Hong-ning,YAN Hong-shun,WANG Chun-gang,LU Xiao-zhu. Effect of lncRNA ADPGK-AS1 on proliferation and apoptosis of non-small cell lung cancer cells by regulating the expression of miR-217[J]. Journal of Clinical Pulmonary Medicine, 2020, 25(7): 998-1004
Authors:XIAO Qin-xiao  CHENG Hong-ning  YAN Hong-shun  WANG Chun-gang  LU Xiao-zhu
Affiliation:(Department of Respiratory Medicine,Qionghai People's Hospital,Qionghai,Hainan 571400,China;Department of Respiratory Medicine,Hainan Provincial People's Hospital,Haikou,Hainan 570311,China)
Abstract:Objective To investigate the levels of lncRNA ADPGK-AS1 and miR-217 in non-small cell lung cancers(NSCLC)tissues and their effect on the proliferation and apoptosis of A549 cells.Methods Taking adjacent tissues as control,the expression levels of lncRNA ADPGK-AS1 and miR-217 in 116 NSCLC tissues were detected by quantitative real-time polymerase chain reactionq(qRT-PCR).The regulatory relationship between lncRNA ADPGK-AS1 and miR-217 were confirmed by dual-luciferase reporting assay system.Si-ADPGK-AS1 and miR-217 were transfected in A549 cells to inhibit lncRNA ADPGK-AS1 and over-expressed miR-217.The proliferation and apoptosis of A549 cells were determined by MTT assay and flow cytometry.The expression of CyclinD1,p21,Bax and Bcl-2 proteins in A549 cells were measured by Western blot.Results Compared with adjacent tissue,the level of lncRNA ADPGK-AS1 in 116 NSCLC tissues was remarkably increased(P<0.05),and the level of miR-217 was significantly decreased(P<0.05).LncRNA ADPGK-AS1 targeted and negatively regulated the expression of miR-217.The inhibition of lncRNA ADPGK-AS1 and over-expression of miR-217 both inhibited the proliferation and promoted the apoptosis of NSCLC A549 cells,reduced the expression levels of CyclinD1 and Bcl-2 in the cells(P<0.05),and increased the levels of p21 and Bax(P<0.05).Interfering of miR-217 reversed the effects of ADPGK-AS1 inhibition on proliferation and apoptosis of A549 cells.Conclusion LncRNA ADPGK-AS1 may promote the proliferation and inhibit apoptosis of NSCLC A549 cells by targeting miR-217.LncRNA ADPGK-AS1 may be a potential molecular target of NSCLC.
Keywords:non-small cell lung cancer  A549 cells  ADP glucokinase antisense RNA 1(ADPGK-AS1)  miR-217  proliferation  apoptosis
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