Bioinformatics and survival analysis of glia maturation factor-γ in pan-cancers.
Bioinformatics and survival analysis of glia maturation factor-γ in pan-cancers.
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泛癌中胶质细胞成熟因子-γ的生物信息学和生存分析
DOI：
10.1186/s12885-021-08163-2
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发表时间：
2021-04-17
期刊：
影响因子：
3.8
通讯作者：
Yang G
中科院分区：
文献类型：
--
作者：
Lan A;Ren C;Wang X;Tong G;Yang G
胶质成熟因子-γ（GMFG）通过与肌动蛋白相关蛋白2/3复合物（Arp 2/3）结合抑制肌动蛋白成核。由于GMFG的主要功能是在肌动蛋白重塑中发挥作用，而肌动蛋白重塑对免疫应答、血管生成、细胞分裂和运动都至关重要，因此认为GMFG在肿瘤发生发展中具有重要作用，但目前只有两项研究描述了GMFG在肿瘤中的作用。本研究利用美国癌症基因组图谱（TCGA）数据对GMFG的临床应用价值进行了研究，并通过对基因本体（GO）和京都基因与基因组百科全书（KEGG）途径丰富内容的分析，探讨了GMFG的作用机制，旨在更好地了解GMFG在泛癌症中的作用，并为GMFG的未来研究提供更多关注。从TCGA收集癌症患者的RNA-seq和临床数据，并通过Kaplan-Meier方法进行分析。GO和KEGG分析使用来自注释、可视化和集成发现数据库（大卫）的在线工具进行。GMFG在胶质母细胞瘤（GBM）、肾透明细胞癌（KIRC）、低级别胶质瘤（LGG）、急性髓性白血病（LAML）、胰腺癌（PAAD）、睾丸癌（TGCT）中表达明显上调，在肾嫌色细胞瘤（KICH）、肺腺癌（LUAD）和肺鳞癌（LUSC）中表达明显下调（P均< 0.05）。GMFG的高表达预示着GBM的OS较差（HR = 1.5，P = 0.017），LGG（HR = 2.2，P < 0.001），LUSC（HR = 1.4，P = 0.022）和眼黑色素瘤（UVM）LGG组（HR = 1.8，P < 0.001）和前列腺癌（PRAD）组（HR = 1.9，P = 0.004）的无病生存率均低于前列腺癌组（HR = 7，P <0.001）。相反，GMFG高表达与皮肤黑色素瘤（SKCM）（HR = 0.59，P < 0.001）和胸腺瘤（THYM）（HR = 0.098，P = 0.031）的较好OS以及胆管癌（CHOL）（HR = 0.2，P = 0.003）的较好DFS相关。GMFG主要参与免疫应答、蛋白结合和嘌呤-细胞因子受体相互作用途径，并且在大多数癌症中与多种免疫调节剂正相关。我们的研究初步发现GMFG可能通过调节肿瘤的进展、免疫应答状态和组织特异性肿瘤微环境（TME）而导致不同癌症的不同生存期。在线版本包含补充材料，可通过10.1186/s12885-021-08163-2获得。
Glia maturation factor-γ (GMFG) is reported to inhibit the actin nucleation through binding to the actin-related protein-2/3 complex (Arp2/3). Considering the main function of GMFG in actin remodeling, which is vital for immune response, angiogenesis, cell division and motility, GMFG is supposed to have important roles in tumor development, while up to now, only two studies described the role of GMFG in cancers. By investigating the clinical values of GMFG using The Cancer Genome Atlas (TCGA) data and the functional mechanisms of GMFG through analyses of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichments, this study was aimed to better understand the impact of GMFG in pan-cancers and to draw more attentions for the future research of GMFG. RNA-seq and clinical data of cancer patients were collected from TCGA and analyzed by the Kaplan-Meier methods. GO and KEGG analyses were conducted using the online tools from the Database for Annotation, Visualization and Integrated Discovery (DAVID). Compared to the corresponding normal samples, GMFG was significantly upregulated in glioblastoma (GBM), kidney clear cell carcinoma (KIRC), lower grade glioma (LGG), acute myeloid leukemia (LAML), and pancreatic cancer (PAAD), testicular cancer (TGCT), but was downregulated in kidney chromophobe (KICH), lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) (P < 0.05 for all). High expression of GMFG predicted worse OS in GBM (HR = 1.5, P = 0.017), LGG (HR = 2.2, P < 0.001), LUSC (HR = 1.4, P = 0.022) and ocular melanomas (UVM) (HR = 7, P < 0.001), as well as worse DFS in LGG (HR = 1.8, P < 0.001) and prostate cancer (PRAD) (HR = 1.9, P = 0.004). In contrast, high expression of GMFG was associated with better OS in skin cutaneous melanoma (SKCM) (HR = 0.59, P < 0.001) and thymoma (THYM) (HR = 0.098, P = 0.031), as well as better DFS in bile duct cancer (CHOL) (HR = 0.2, P = 0.003). GMFG was mainly involved in the immune response, protein binding and cytokine-cytokine receptor interaction pathways, and was positively associated with multiple immunomodulators in most cancers. Our study preliminarily identified that GMFG may cause different survivals for different cancers through modulating tumor progression, immune response status and tissue-specific tumor microenvironment (TME). The online version contains supplementary material available at 10.1186/s12885-021-08163-2.
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