CCNB2对肺腺癌的诊断及调控功能研究

Diagnostic value and regulatory function of CCNB2 in lung adenocarcinoma

    摘要
  • 摘要:
    目的 研究细胞周期蛋白B2（CCNB2）对于肺腺癌（lung adenocarcinoma，LUAD）的诊断价值及其调控功能。
    方法 收集2016年10月至2019年10月淮安市淮安医院就诊的100例LUAD患者标本，用以检测CCNB2在临床组织中的表达。通过受试者工作特性曲线（receiver operating characteristic，ROC）分析CCNB2在LUAD中的诊断价值。基于癌症基因组图谱（TCGA）数据库分析CCNB2表达与临床分期的关系。通过实时荧光定量逆转录聚合酶链反应（quantitative reverse transcription polymerase chain reaction，qRT-PCR）和蛋白免疫印迹（Western blot，WB）检测CCNB2在LUAD细胞和正常细胞中各自的表达量，WB检测细胞和肿瘤组织中细胞周期蛋白。通过克隆形成、CCK-8、侵袭和划痕愈合实验研究CCNB2对LUAD细胞的增殖、侵袭和迁移的影响。流式细胞术检测细胞周期。
    结果 相较于正常肺腺组织，CCNB2在LUAD组织中的表达量显著增高。ROC曲线显示曲线下面积（AUC）值为0.902，表明CCNB2对于LUAD具有良好的诊断价值。CCNB2在LUAD中高表达；沉默CCNB2能够抑制LUAD的增殖、侵袭和迁移，并阻滞细胞周期在G0/G1期。沉默CCNB2能够抑制小鼠体内LUAD的进展。
    结论 CCNB2可以作为LUAD的诊断标志物，并且下调CCNB2表达后可以抑制LUAD细胞的增殖、侵袭和迁移，表明其可作为治疗LUAD的潜在靶点。

     

    Abstract:
    Objective To investigate the diagnostic value and regulatory function of Cyclin B2 (CCNB2) in lung adenocarcinoma (LUAD).
    Methods One hundred specimens from patients with LUAD who were admitted to the Huai'an Hospital between October 2016 and October 2019 were collected to detect the expression of CCNB2 in clinical tissues. The diagnostic value of CCNB2 in LUAD was analyzed using receiver operating characteristic (ROC) curves. The relationship between CCNB2 expression and clinical stage was analyzed based on The Cancer Genome Atlas (TCGA) database. The expression levels of CCNB2 in LUAD and normal cells were detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot (WB). Cell cycle proteins were also detected in the cells and cancer tissues using Western blot. The effects of CCNB2 on the proliferation, invasion, and migration of LUAD cells were detected using colony formation, CCK-8, Transwell, and wound healing assays. The cell cycle was analyzed using flow cytometry.
    Results CCNB2 expression was significantly higher in LUAD tissues than that in normal tissues. The area under the curve (AUC) was 0.902, indicating that CCNB2 had a good diagnostic value for LUAD. Silencing CCNB2 inhibited the proliferation, invasion, and migration of LUAD cells and blocked the cell cycle in the G0/G1 phase. Silencing CCNB2 inhibit progression of lung adenocarcinoma in mice.
    Conclusions CCNB2 can be a diagnostic marker for LUAD, and the downregulation of CCNB2 expression can inhibit the proliferation, invasion, and migration of LUAD cells, indicating its potential as a therapeutic target for LUAD.

     

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