ETV4转录因子癌基因的生物信息学筛选和小分子抗癌药物的鉴定,Chemical Biology & Drug Design

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ETV4转录因子癌基因的生物信息学筛选和小分子抗癌药物的鉴定
Chemical Biology & Drug Design ( IF 3.2 ) Pub Date : 2021-11-10 , DOI: 10.1111/cbdd.13981
Ambily Nath I V ₁ , Achuthsankar S Nair ₁

Affiliation

这项生物信息学研究旨在鉴定 ETV4 转录因子致癌基因并概述这些基因的抗癌药物。首先，我们收集了已知的 61 个 ETV4 癌症目标，这些目标被构建为两类查询，以筛选 GeneMANIA 中的多组学资源。该方法访问并在每组中添加了功能相似的 20 个基因。这些数据通过中枢基因、网络聚类、基因本体和通路分析进行解释，结果证实所有产生的基因都是癌症启动子。从这些基因的启动子区域鉴定出 ETS 结合基序。因此，计算出 23 个 ETV4 目标，并且将参与肿瘤发生的目标过滤为以下 16 个推定节点：MMP8、MMP14、KDR、BRIP1、CXCR1、GRB14、SHC2、SHC4、SH2B1、SH2B2、INPPL1、PTPN3、GNG12、SEMA4D、RHOA和SPSB2。这些癌基因的转录调控是由一个广泛的 miRNA 网络协调的，该网络发现可以解除对许多癌症通路的调控。使用 DgIb 数据库，高质量的 6 种癌基因药物组合（MMP8 -CHEMBL1231240、MMP8 -Aminomethylamide、CXCR1 -Reparixin、SEMA4D -Pepinemab、RHOA -Clausine E 和SPSB2 -CHEMBL175296）被提出。这些发现可能会促进我们对 ETV4 的新肿瘤基因关系的理解，并为其调节设计治疗策略。

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Bioinformatics screening of ETV4 transcription factor oncogenes and identifying small-molecular anticancer drugs

This bioinformatics study aimed to identify ETV4 transcription factor oncogenes and outline anticancer drugs for these genes. First, we collected known 61 ETV4 cancer targets that were framed as two classes of queries to screen against the multiomics resources in GeneMANIA. This method accessed and added functionally similar 20 genes to each set. These data were interpreted by hub genes, network clustering, gene ontology, and pathway analyses, and the results confirmed that all resultant genes were cancer promoters. The ETS-binding motifs were identified from the promoter regions of these genes. Thus, 23 ETV4 targets were figured and those involved in oncogenesis were filtered as the following 16 putative nodes: MMP8, MMP14, KDR, BRIP1, CXCR1, GRB14, SHC2, SHC4, SH2B1, SH2B2, INPPL1, PTPN3, GNG12, SEMA4D, RHOA, and SPSB2. The transcriptional regulation of these oncogenes was coordinated by an extensive miRNA network that found to deregulate many cancer pathways. Using DgIb database, the high quality 6 oncogene-drug combinations (MMP8-CHEMBL1231240, MMP8-Aminomethylamide, CXCR1-Reparixin, SEMA4D-Pepinemab, RHOA-Clausine E, and SPSB2-CHEMBL175296) were proposed. These findings may advance our understanding of novel neoplastic gene nexus of ETV4 and design treatment strategies for its modulation.

更新日期：2021-11-10

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