Department of Urology, The Third Affiliated Hospital of Soochow University, No. 185, Juqian Street, Changzhou City, Jiangsu Province, China; Department of Urology, Xuzhou Clinical School of Xuzhou Medical College, Xuzhou Central Hospital, No. 199 Jiefang South Road, Xuzhou, Jiangsu, China.
Department of Urology, Xuzhou Clinical School of Xuzhou Medical College, Xuzhou Central Hospital, No. 199 Jiefang South Road, Xuzhou, Jiangsu, China.
Gene. 2020 May 15;738:144475. doi: 10.1016/j.gene.2020.144475. Epub 2020 Feb 17.
In this article, we utilized Ingenuity® Pathway Analysis (IPA®) bioinformatics analysis software and Metascape® bioinformatics analysis website tools to analyse the possible mechanism of ERH affecting tumourigenesis (proliferation and apoptosis) in bladder cancer (BC) T24 cells.
The ERH gene was knocked down, and BC T24 cells were divided into ERH normal and knockdown groups. Affymetrix® gene expression microarrays were performed to obtain a differentially expressed gene list (DEGL) between the 2 groups. IPA® data analyses contain five modules: disease and function analysis, upstream analysis, regulator effects analysis, canonical pathway analysis and molecular network analysis. The results of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were analysed by Metascape®.
The results of the gene expression profiling chip and the DEGL showed that 344 genes were upregulated and 254 genes were downregulated. The IPA® and Metascape® pathway analyses showed that the ERH gene may affect proliferation and apoptosis by affecting the apoptosis, cell cycle, Toll-like receptor (TLR), NF-κB or TGF-beta signalling pathways. Upstream analysis determined that the ERH gene may regulate TNF and NK-κB in the BC T24 cell lines. The ERH gene may be involved in the "cell death and survival" molecular network in BC T24 cells. ERH may be a regulator of KITLG through TNF.
The ERH gene may affect apoptosis through the TLR, NF-κB, TNF or TGF-beta signalling pathways in BC T24 cells, and may be a regulator of KITLG to ultimately activate the growth of malignant tumours.
在本文中，我们利用 Ingenuity® Pathway Analysis（IPA®）生物信息学分析软件和 Metascape®生物信息学分析网站工具，分析 ERH 影响膀胱癌（BC）T24 细胞肿瘤发生（增殖和凋亡）的可能机制。
敲低 ERH 基因，将 BC T24 细胞分为 ERH 正常和敲低组。使用 Affymetrix®基因表达微阵列获得两组间差异表达基因列表（DEGL）。IPA®数据分析包含五个模块：疾病和功能分析、上游分析、调控因子效应分析、经典途径分析和分子网络分析。Gene Ontology（GO）和 Kyoto Encyclopedia of Genes and Genomes（KEGG）富集分析结果通过 Metascape®进行分析。
基因表达谱芯片和 DEGL 的结果显示，有 344 个基因上调，254 个基因下调。IPA®和 Metascape®通路分析表明，ERH 基因可能通过影响凋亡、细胞周期、Toll 样受体（TLR）、NF-κB 或 TGF-β信号通路来影响增殖和凋亡。上游分析确定 ERH 基因可能在 BC T24 细胞系中调节 TNF 和 NK-κB。ERH 基因可能参与 BC T24 细胞中的“细胞死亡和存活”分子网络。ERH 可能通过 TNF 调节 KITLG。
ERH 基因可能通过 TLR、NF-κB、TNF 或 TGF-β信号通路影响 BC T24 细胞中的凋亡，可能是 KITLG 的调节因子，最终激活恶性肿瘤的生长。
