Potential biomarkers and signaling pathways associated with the pathogenesis of primary salivary gland carcinoma: a bioinformatics study.

Q2 Agricultural and Biological Sciences Genomics and Informatics Pub Date : 2021-12-01 Epub Date: 2021-12-31 DOI:10.5808/gi.21052
Zeynab Bayat, Fatemeh Ahmadi-Motamayel, Mohadeseh Salimi Parsa, Amir Taherkhani
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引用次数: 6

Abstract

Salivary gland carcinoma (SGC) is rare cancer, constituting 6% of neoplasms in the head and neck area. The most responsible genes and pathways involved in the pathology of this disorder have not been fully understood. We aimed to identify differentially expressed genes (DEGs), the most critical hub genes, transcription factors, signaling pathways, and biological processes (BPs) associated with the pathogenesis of primary SGC. The mRNA dataset GSE153283 in the Gene Expression Omnibus database was re-analyzed for determining DEGs in cancer tissue of patients with primary SGC compared to the adjacent normal tissue (adjusted p-value < 0.001; |Log2 fold change| > 1). A protein interaction map (PIM) was built, and the main modules within the network were identified and focused on the different pathways and BP analyses. The hub genes of PIM were discovered, and their associated gene regulatory network was built to determine the master regulators involved in the pathogenesis of primary SGC. A total of 137 genes were found to be differentially expressed in primary SGC. The most significant pathways and BPs that were deregulated in the primary disease condition were associated with the cell cycle and fibroblast proliferation procedures. TP53, EGF, FN1, NOTCH1, EZH2, COL1A1, SPP1, CDKN2A, WNT5A, PDGFRB, CCNB1, and H2AFX were demonstrated to be the most critical genes linked with the primary SGC. SPIB, FOXM1, and POLR2A significantly regulate all the hub genes. This study illustrated several hub genes and their master regulators that might be appropriate targets for the therapeutic aims of primary SGC.

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原发性唾液腺癌发病机制的潜在生物标志物和信号通路:一项生物信息学研究。
唾液腺癌(SGC)是一种罕见的癌症,占头颈部肿瘤的6%。参与这种疾病病理的最负责任的基因和途径尚未完全了解。我们旨在确定与原发性SGC发病机制相关的差异表达基因(DEGs)、最关键的枢纽基因、转录因子、信号通路和生物学过程(bp)。重新分析基因表达综合数据库中的mRNA数据集GSE153283,以确定原发性SGC患者的癌组织中与邻近正常组织中的DEGs(调整p值< 0.001;构建了蛋白质相互作用图谱(PIM),并对网络中的主要模块进行了识别,重点进行了不同途径和BP分析。我们发现了PIM的枢纽基因,并构建了相关基因调控网络,确定了参与原发性SGC发病机制的主要调控因子。在原发性SGC中,共有137个基因存在差异表达。在原发疾病条件下最重要的通路和bp被解除调控与细胞周期和成纤维细胞增殖过程相关。TP53、EGF、FN1、NOTCH1、EZH2、COL1A1、SPP1、CDKN2A、WNT5A、PDGFRB、CCNB1和H2AFX被证明是与原发性SGC相关的最关键基因。SPIB、FOXM1和POLR2A显著调控所有枢纽基因。本研究阐明了几个中枢基因及其主调控因子可能是原发性SGC治疗目的的合适靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Genomics and Informatics
Genomics and Informatics Agricultural and Biological Sciences-Ecology, Evolution, Behavior and Systematics
CiteScore
1.90
自引率
0.00%
发文量
0
审稿时长
12 weeks
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