Zarei-Ghobadi Mohadeseh, Sheikhi Mohsen, Teymoori-Rad Majid, Yaslianifard Sahar, Norouzi Mehdi, Yaslianifard Somayeh, Faraji Reza, Farahmand Mohammad, Bayat Shiva, Jafari Mohieddin, Mozhgani Sayed-Hamidreza
Institute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran.
Department of Biochemistry, Faculty of Life Sciences of Islamic, Azad University, Tehran north branch, Tehran, Iran.
BMC Res Notes. 2021 Mar 23;14(1):109. doi: 10.1186/s13104-021-05521-y.
Human T cell leukemia virus-1 (HTLV-1) infection may lead to one or both diseases including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) or adult T cell leukemia lymphoma (ATLL). The complete interactions of the virus with host cells in both diseases is yet to be determined. This study aims to construct an interaction network for distinct signaling pathways in these diseases based on finding differentially expressed genes (DEGs) between HAM/TSP and ATLL.
We identified 57 hub genes with higher criteria scores in the primary protein-protein interaction network (PPIN). The ontology-based enrichment analysis revealed following important terms: positive regulation of transcription from RNA polymerase II promoter, positive regulation of transcription from RNA polymerase II promoter involved in meiotic cell cycle and positive regulation of transcription from RNA polymerase II promoter by histone modification. The upregulated genes TNF, PIK3R1, HGF, NFKBIA, CTNNB1, ESR1, SMAD2, PPARG and downregulated genes VEGFA, TLR2, STAT3, TLR4, TP53, CHUK, SERPINE1, CREB1 and BRCA1 were commonly observed in all the three enriched terms in HAM/TSP vs. ATLL. The constructed interaction network was then visualized inside a mirrored map of signaling pathways for ATLL and HAM/TSP, so that the functions of hub genes were specified in both diseases.
人类T细胞白血病病毒1型(HTLV-1)感染可能导致一种或两种疾病,包括HTLV-1相关脊髓病/热带痉挛性截瘫(HAM/TSP)或成人T细胞白血病淋巴瘤(ATLL)。该病毒与这两种疾病中宿主细胞的完整相互作用尚未确定。本研究旨在基于发现HAM/TSP和ATLL之间的差异表达基因(DEG),构建这两种疾病中不同信号通路的相互作用网络。
我们在初级蛋白质-蛋白质相互作用网络(PPIN)中鉴定出57个具有较高标准分数的枢纽基因。基于本体的富集分析揭示了以下重要术语:RNA聚合酶II启动子转录的正调控、参与减数分裂细胞周期的RNA聚合酶II启动子转录的正调控以及组蛋白修饰对RNA聚合酶II启动子转录的正调控。上调基因TNF、PIK3R1、HGF、NFKBIA、CTNNB1、ESR1、SMAD2、PPARG和下调基因VEGFA、TLR2、STAT3、TLR4、TP53、CHUK、SERPINE1、CREB1和BRCA1在HAM/TSP与ATLL的所有三个富集术语中均普遍观察到。然后,在ATLL和HAM/TSP信号通路的镜像图中可视化构建的相互作用网络,以便在两种疾病中明确枢纽基因的功能。