PDF(Pubmed)
Abstract：
UNASSIGNED: Ameloblastoma (AM) is a benign tumor locally originated from odontogenic epithelium that is commonly found in the jaw. This tumor makes aggressive invasions and has a high recurrence rate. This study aimed to investigate the differentially expressed genes (DEGs), biological function alterations, disease targets, and existing drugs for AM using bioinformatics analysis.
UNASSIGNED: The data set of AM was retrieved from the GEO database (GSE132474) and identified the DEGs using bioinformatics analysis. The biological alteration analysis was applied to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Protein-protein interaction (PPI) network analysis and hub gene identification were screened through NetworkAnalyst. The transcription factor-protein network was constructed via OmicsNet. We also identified candidate compounds from L1000CDS2 database. The target of AM and candidate compounds were verified using docking simulation.
UNASSIGNED: Totally, 611 DEGs were identified. The biological function enrichment analysis revealed glycosaminoglycan and GABA (γ-aminobutyric acid) signaling were most significantly up-regulated and down-regulated in AM, respectively. Subsequently, hub genes and transcription factors were screened via the network and showed FOS protein was found in both networks. Furthermore, we evaluated FOS protein to be a therapeutic target in AMs. Candidate compounds were screened and verified using docking simulation. Tanespimycin showed the greatest affinity binding value to bind FOS protein.
UNASSIGNED: This study presented the underlying molecular mechanisms of disease pathogenesis, biological alteration, and important pathways of AMs and provided a candidate compound, Tanespimycin, targeting FOS protein for the treatment of AMs.
UNASSIGNED: The data set of AM was retrieved from the GEO database (GSE132474) and identified the DEGs using bioinformatics analysis. The biological alteration analysis was applied to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Protein-protein interaction (PPI) network analysis and hub gene identification were screened through NetworkAnalyst. The transcription factor-protein network was constructed via OmicsNet. We also identified candidate compounds from L1000CDS2 database. The target of AM and candidate compounds were verified using docking simulation.
UNASSIGNED: Totally, 611 DEGs were identified. The biological function enrichment analysis revealed glycosaminoglycan and GABA (γ-aminobutyric acid) signaling were most significantly up-regulated and down-regulated in AM, respectively. Subsequently, hub genes and transcription factors were screened via the network and showed FOS protein was found in both networks. Furthermore, we evaluated FOS protein to be a therapeutic target in AMs. Candidate compounds were screened and verified using docking simulation. Tanespimycin showed the greatest affinity binding value to bind FOS protein.
UNASSIGNED: This study presented the underlying molecular mechanisms of disease pathogenesis, biological alteration, and important pathways of AMs and provided a candidate compound, Tanespimycin, targeting FOS protein for the treatment of AMs.
摘要：
■成釉细胞瘤（AM）是一种良性肿瘤，局部起源于牙源性上皮，常见于颌骨。这种肿瘤具有侵袭性侵袭性，复发率高。本研究旨在探讨差异表达基因(DEGs),生物功能改变，疾病目标,和现有的AM药物使用生物信息学分析。
■从GEO数据库（GSE132474）检索AM的数据集，并使用生物信息学分析识别DEGs。将生物学改变分析应用于基因本体论（GO）和京都基因和基因组百科全书（KEGG）途径。通过NetworkAnalyst筛选蛋白质-蛋白质相互作用（PPI）网络分析和hub基因鉴定。通过OmicsNet构建转录因子-蛋白质网络。我们还从L1000CDS2数据库鉴定了候选化合物。利用对接模拟验证了AM和候选化合物的目标。
■完全,识别出611个DEG。生物学功能富集分析显示糖胺聚糖和γ-氨基丁酸(GABA)信号在AM中表达上调和下调最为显著,分别。随后，通过网络筛选了hub基因和转录因子，并显示在两个网络中都发现了FOS蛋白。此外，我们评估了FOS蛋白是AMs的治疗靶标。使用对接模拟筛选和验证候选化合物。Tanespimycin对结合FOS蛋白显示出最大的亲和力结合值。
■这项研究提出了疾病发病机制的潜在分子机制，生物改变,和AMs的重要途径，并提供了候选化合物，Tanespimocin,靶向FOS蛋白治疗AMs。
■从GEO数据库（GSE132474）检索AM的数据集，并使用生物信息学分析识别DEGs。将生物学改变分析应用于基因本体论（GO）和京都基因和基因组百科全书（KEGG）途径。通过NetworkAnalyst筛选蛋白质-蛋白质相互作用（PPI）网络分析和hub基因鉴定。通过OmicsNet构建转录因子-蛋白质网络。我们还从L1000CDS2数据库鉴定了候选化合物。利用对接模拟验证了AM和候选化合物的目标。
■完全,识别出611个DEG。生物学功能富集分析显示糖胺聚糖和γ-氨基丁酸(GABA)信号在AM中表达上调和下调最为显著,分别。随后，通过网络筛选了hub基因和转录因子，并显示在两个网络中都发现了FOS蛋白。此外，我们评估了FOS蛋白是AMs的治疗靶标。使用对接模拟筛选和验证候选化合物。Tanespimycin对结合FOS蛋白显示出最大的亲和力结合值。
■这项研究提出了疾病发病机制的潜在分子机制，生物改变,和AMs的重要途径，并提供了候选化合物，Tanespimocin,靶向FOS蛋白治疗AMs。
