首页|LINC02535/miR-30b/CCNA2轴通过抑制细胞凋亡和促进增殖参与肺腺癌的发生和发展

LINC02535/miR-30b/CCNA2轴通过抑制细胞凋亡和促进增殖参与肺腺癌的发生和发展

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目的 旨在探究LINC02535/miR-30b/CCNA2轴在肺腺癌(lungadenocarcinoma,LUAD)发生和发展中的作用机制,通过分析基因表达情况发现相关分子标志物和信号通路,并验证其作用.方法 从癌症基因组图谱(TCGA)中获取LUAD的lncRNA、miRNA和mRNA的表达谱数据和临床数据,利用R3.6.0软件的"edgeR"差异分析数据包筛选差异表达基因,进一步利用R3.6.0软件的"WGCNA"数据包进行加权基因共表达网络分析,得到构成ceRNA的基因共表达网络图.同时,对2种人LUAD细胞系A549、H1299和1种标准支气管上皮细胞系BEAS-2B进行细胞培养和转染,使用qRT-PCR、CCK-8、EdU分析和细胞周期分析等方法评估细胞增殖.结果 从TCGA数据库中获取了高表达的lncRNA、低表达的miRNA和高表达的mRNA,通过加权基因共表达网络分析筛选出20个生存分析预后显著差异的lncRNA.其中,LINC02535与miR-30b呈负相关,并且存在结合靶点.进一步研究发现,LINC02535在LUAD组织和细胞系中显著过表达,而miR-30b则显著低表达.通过降低LINC02535的表达水平,发现其对细胞增殖有抑制作用.此外,降低LINC02535的表达水平还发现其对细胞凋亡和G1向S期转变有抑制作用.同时,LINC02535下调导致miR-30b的表达升高,使得CCNA2的表达下降.结论 LINC02535/miR-30b/CCNA2轴通过抑制细胞凋亡和促进增殖参与了 LUAD的发生和发展,可能成为潜在治疗LUAD的分子靶点.
LINC02535/miR-30b/CCNA2 axis participates in the pathogensis of lung adenocarcinoma by inhibiting apoptosis and promoting proliferation
Objective To explore the role of the LINC02535/miR-30b/CCNA2 axis in the pathogenesis of lung adenocarcinoma(LUAD),and identify relevant molecular markers and signaling pathways by analyzing gene expression and verify their effects.Methods The gene expression profiles of lncRNA,miRNA,and mRNA in LUAD and related clinical data were obtained from the Cancer Genome Atlas(TCGA),and differentially expressed genes were screened using the"edgeR"differential analysis package in R3.6.0 software.Furthermore,weighted gene co-expression network analysis was performed using the"WGCNA"package in R3.6.0 software to establish a gene co-expression network map of ceRNA.Meanwhile,two human LUAD cell lines A549 and H1299 and one standard bronchial epithelial cell line(BEAS-2B)were cultivated for transfection.Cell proliferation was evaluated by qRT-PCR,CCK-8 assay,EdU assay,and cell cycle analysis.Results From the TCGA database,high-expression lncRNAs,low-expression miRNAs,and high-expression mRNAs were obtained.Through weighted gene co-expression network analysis,20 lncRNAs with significant differences in survival analysis were screened out.Among them,LINC02535 showed a significant negative correlation with miR-30b,with binding targets.Further research found that LINC02535 was overexpressed in LUAD tissues and cell lines,while miR-30b was significantly down-regulated.Reduced expression of LINC02535 resulted in inhibitory effect on cell proliferation,cell apoptosis and G1 to S phase transition.Meanwhile,down-regulation of LINC02535 led to increased expression of miR-30b,and then decreased the expression of CCNA2.Conclusions The LINC02535/miR-30b/CCNA2 axis participates in the pathogenesis of LUAD by inhibiting apoptosis and promoting proliferation,which may become a potential molecular target for treating LUAD.

lung adenocarcinomalncRNALINC02535ceRNAproliferationcell cycle

顾一航、缪健、王琳、殷泉忠、王兰

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徐州医科大学江阴临床学院老年医学科,江苏江阴 214400

肺腺癌 lncRNA LINC02535 ceRNA 增殖 细胞周期

国家自然科学基金青年基金徐州医科大学附属医院发展基金江苏省重点实验室开放研究课题无锡市卫生健康委中青年拔尖人才资助计划江阴市中青年卫生优秀人才资助计划

82000012XYFY2020006XZSYSKF2020021BJ2023101JYOYT202301

2024

徐州医科大学学报
徐州医学院

徐州医科大学学报

CSTPCD
影响因子:0.395
ISSN:2096-3882
年,卷(期):2024.44(2)
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