Department of Radiology, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.
Department of Neurosurgery, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.
Mol Med Rep. 2017 Oct;16(4):5561-5567. doi: 10.3892/mmr.2017.7216. Epub 2017 Aug 10.
The present study aimed to investigate gene expression profile alterations associated with cysteine‑rich 61 (CYR61) expression in human glioma cells. The GSE29384 dataset, downloaded from the Gene Expression Omnibus, includes three LN229 human glioma cell samples expressing CYR61 induced by doxycycline (Dox group), and three control samples not exposed to doxycycline (Nodox group). Differentially expressed genes (DEGs) between the Dox and Nodox groups were identified with cutoffs of |log2 fold change (FC)|>0.5 and P<0.05. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses for DEGs were performed. Protein‑protein interaction (PPI) network and module analyses were performed to identify the most important genes. Transcription factors (TFs) were obtained by detecting the TF binding sites of DEGs using a Whole Genome rVISTA online tool. A total of 258 DEGs, including 230 (89%) upregulated and 28 (11%) downregulated DEGs were identified in glioma cells expressing CYR61 compared to cells without CYR61 expression. The majority of upregulated DEGs, including interferon (IFN)B1, interferon‑induced (IFI)44 and interferon regulatory factor (IRF)7, were associated with immune, defense and virus responses, and cytokine‑cytokine receptor interaction signaling pathways. Signal transducer and activator of transcription 1 (STAT1) and DEAD‑box helicase 58 (DDX58) were observed to have high connection degrees in the PPI network. A total of seven TFs of the DEGs, including interferon consensus sequence‑binding protein and IFN‑stimulated gene factor‑3 were additionally detected. In conclusion, IFNB1, genes encoding IFN‑induced proteins (IFI16, IFI27, IFI44 and IFITM1), IRFs (IRF1, IRF7 and IRF9), STAT1 and DDX58 were demonstrated to be associated with CYR61 expression in glioma cells; thus, they may be critical for maintaining the role of CYR61 during cancer progression.
本研究旨在探讨与人类神经胶质瘤细胞中半胱氨酸丰富蛋白 61（CYR61）表达相关的基因表达谱改变。从基因表达综合数据库中下载的 GSE29384 数据集包括三个经强力霉素（Dox）诱导表达 CYR61 的 LN229 人神经胶质瘤细胞样本（Dox 组），以及三个未暴露于强力霉素的对照样本（Nodox 组）。通过设定 |log2 倍变化（FC）|>0.5 和 P<0.05 的截值，鉴定 Dox 组和 Nodox 组之间的差异表达基因（DEGs）。对 DEGs 进行基因本体论和京都基因与基因组百科全书通路富集分析。通过使用全基因组 rVISTA 在线工具检测 DEGs 的转录因子（TF）结合位点，进行蛋白-蛋白相互作用（PPI）网络和模块分析，以鉴定最重要的基因。通过 Whole Genome rVISTA 在线工具检测 DEGs 的 TF 结合位点，获得转录因子（TFs）。与未表达 CYR61 的细胞相比，表达 CYR61 的神经胶质瘤细胞中鉴定出 258 个差异表达基因（DEGs），其中 230 个（89%）上调，28 个（11%）下调。大多数上调的 DEGs，包括干扰素（IFN）B1、干扰素诱导（IFI）44 和干扰素调节因子（IRF）7，与免疫、防御和病毒反应以及细胞因子-细胞因子受体相互作用信号通路有关。在 PPI 网络中观察到信号转导和转录激活因子 1（STAT1）和 DEAD-box 解旋酶 58（DDX58）具有较高的连接度。共检测到 7 个 DEGs 的 TF，包括干扰素共识序列结合蛋白和 IFN 刺激基因因子 3。总之，IFNB1、编码干扰素诱导蛋白（IFI16、IFI27、IFI44 和 IFITM1）、IRFs（IRF1、IRF7 和 IRF9）、STAT1 和 DDX58 的基因与神经胶质瘤细胞中 CYR61 的表达有关；因此，它们可能对维持 CYR61 在癌症进展过程中的作用至关重要。
