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基于生物信息学分析的NSC319726在卵巢癌中的作用

Role of NSC319726 in ovarian cancer based on the bioinformatics analyses.

作者信息

Xue Ji, Yang Guang, Ding Hong, Wang Pu, Wang Changhong

机构信息

Department of Chinese Medicine, The Second Hospital of Jilin University, People's Republic of China.

The Clinical Medical College of Jilin University (Grade 2013), People's Republic of China.

出版信息

Onco Targets Ther. 2015 Dec 15;8:3757-65. doi: 10.2147/OTT.S86343. eCollection 2015.

Abstract

AIM

This study aimed to explore the molecular mechanisms of NSC319726 in ovarian cancer by bioinformatics analyses.

METHODS

Gene expression profile GSE35972 was downloaded from the Gene Expression Omnibus database. The data set contains six samples, including three samples of TOV112D cells untreated and three samples of TOV112D cells treated with NSC319726. The differentially expressed genes (DEGs) between untreated and treated samples were analyzed using the limma package. Kyoto Encyclopedia of Genes and Genomes pathway analysis was performed using the signaling pathway impact analysis package, followed by the functional annotation of DEGs and protein-protein interaction network construction. Finally, the subnetwork was identified, and Gene Ontology functional enrichment analysis was performed on the DEGs enriched in the subnetwork.

RESULTS

A total of 120 upregulated and 126 downregulated DEGs were identified. Six Kyoto Encyclopedia of Genes and Genomes pathways were significantly perturbed by DEGs, and the pathway of oocyte meiosis was identified as the most perturbed one. Oocyte meiosis was enriched by eight downregulated DEGs, such as ribosomal protein S6 kinase, 90 kDa, and polypeptide 6 (RPS6KA6). After functional annotation, eight transcription factors were upregulated (such as B-cell CLL/lymphoma 6 [BCL6]), and three transcription factors were downregulated. Seven tumor suppressor genes, such as forkhead box O3 (FOXO3), were upregulated. Additionally, in the protein-protein interaction network and subnetwork, cyclin B1 (CCNB1) and cell division cycle 20 (CDC20) were hub genes, which were also involved in the functions related to mitotic cell cycle.

CONCLUSION

NSC319726 may play an efficient role against ovarian cancer via targeting genes, such as RPS6KA6, BCL6, FOXO3, CCNB1, and CDC20, which are involved in oocyte meiosis pathway.

摘要

目的

本研究旨在通过生物信息学分析探索NSC319726在卵巢癌中的分子机制。

方法

从基因表达综合数据库下载基因表达谱GSE35972。该数据集包含六个样本,包括三个未处理的TOV112D细胞样本和三个用NSC319726处理的TOV112D细胞样本。使用limma软件包分析未处理和处理样本之间的差异表达基因(DEG)。使用信号通路影响分析软件包进行京都基因与基因组百科全书通路分析,随后对DEG进行功能注释并构建蛋白质-蛋白质相互作用网络。最后,识别子网,并对子网中富集的DEG进行基因本体功能富集分析。

结果

共鉴定出120个上调和126个下调的DEG。六个京都基因与基因组百科全书通路受到DEG的显著干扰,卵母细胞减数分裂通路被确定为受干扰最严重的通路。卵母细胞减数分裂由八个下调的DEG富集,如核糖体蛋白S6激酶90 kDa多肽6(RPS6KA6)。功能注释后,八个转录因子上调(如B细胞淋巴瘤/白血病6 [BCL6]),三个转录因子下调。七个肿瘤抑制基因,如叉头框O3(FOXO3)上调。此外,在蛋白质-蛋白质相互作用网络和子网中,细胞周期蛋白B1(CCNB1)和细胞分裂周期20(CDC20)是枢纽基因,它们也参与与有丝分裂细胞周期相关的功能。

结论

NSC319726可能通过靶向参与卵母细胞减数分裂途径的基因,如RPS6KA6、BCL6、FOXO3、CCNB1和CDC20,对卵巢癌发挥有效作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9d/4689271/9b6c6ff66e63/ott-8-3757Fig1.jpg

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