Karyopherin subunit-α 2 expression accelerates cell cycle progression by upregulating CCNB2 and CDK1 in hepatocellular carcinoma.
Karyopherin subunit-α 2 expression accelerates cell cycle progression by upregulating CCNB2 and CDK1 in hepatocellular carcinoma.
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核蛋白亚基-α2表达通过上调肝细胞癌中的CCNB2和CDK1来加速细胞周期的进程。
DOI：
10.3892/ol.2017.7691
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发表时间：
2018-03
期刊：
影响因子：
2.9
通讯作者：
Zhuang L
中科院分区：
文献类型：
--
作者：
Gao CL;Wang GW;Yang GQ;Yang H;Zhuang L
不同类型的癌症表现出不同的基因表达谱。本研究旨在确定在肝细胞癌(肝细胞癌)中调节失调的特定基因，该基因在肿瘤进展中是必不可少的。用基因芯片分析原代肝细胞癌组织样本的全部转录本。确定了差异表达最显著的基因，特别是核粘附素亚基-α2(KPNA2)，并使用Oncomine在线工具对来自癌症基因组图谱的数据进行分析，以预测肝癌的相关基因。逆转录-定量聚合酶链式反应证实KPNA2基因的表达水平，并通过RNA干扰敲除KPNA2对可能的下游靶基因的影响。采用细胞增殖实验和流式细胞术分析KPNA2在细胞周期调控中的作用。结果表明，KPNA2在肝细胞癌组织中的表达显著高于肝组织，并与细胞周期蛋白B2(CCNB2)和细胞周期蛋白依赖性激酶1(CDK1)的表达密切相关。KPNA2的表达被认为是一种新的预测患者预后的标志物。此外，KPNA2基因敲除下调了CCNB2和CDK1的表达，抑制了细胞增殖，并诱导细胞周期停滞于G2/M期。提示KPNA2可能通过上调CCNB2/CDK1的表达来促进肿瘤细胞的增殖。KPNA2可能成为肝细胞癌治疗干预的靶点。
Different types of cancer exhibit distinct gene expression profiles. The present study aimed to identify a specific gene dysregulated in hepatocellular carcinoma (HCC) that was essential for cancer progression. The whole transcriptomes of primary HCC tissue samples were analyzed with microarrays. The most significantly differentially expressed gene was identified, specifically karyopherin subunit-α 2 (KPNA2), and an analysis using the Oncomine online tool was performed with data from The Cancer Genome Atlas to predict associated genes in HCC. Reverse transcription-quantitative polymerase chain reaction was performed to confirm the gene expression levels of KPNA2, and the RNA interference knockdown of KPNA2 was performed to identify the effect on putative downstream target genes. A proliferation assay and flow cytometry analysis was used to assess the function of KPNA2 in the regulation of the cell cycle. The results demonstrated that KPNA2 expression was significantly upregulated in HCC tumor tissues compared with liver tissues and was associated with cyclin B2 (CCNB2) and cyclin-dependent kinase 1 (CDK1) expression. KPNA2 expression was identified a novel marker to predict the outcome of patients. In addition, KPNA2 knockdown downregulated CCNB2 and CDK1, inhibited cell proliferation and induced cell cycle arrest in the G2/M phase. In conclusion, it was demonstrated that KPNA2 may promote tumor cell proliferation by increasing the expression of CCNB2/CDK1. KPNA2 could be a target for therapeutic intervention in HCC.
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