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SPI1-TYROBP-FCER1G 网络在骨肉瘤发生发展和预后中的作用及其与免疫浸润的关系

The role of SPI1-TYROBP-FCER1G network in oncogenesis and prognosis of osteosarcoma, and its association with immune infiltration.

机构信息

Department of Orthopedics, Hefei BOE Hospital, Hefei, Anhui, China.

Department of Immunology, School of Basic Medical Sciences, Anhui Medical University, No.81Mei Shan Road, Hefei, 230032, Anhui, China.

出版信息

BMC Cancer. 2022 Jan 25;22(1):108. doi: 10.1186/s12885-022-09216-w.

DOI:10.1186/s12885-022-09216-w
PMID:35078433
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8790913/
Abstract

Osteosarcoma is an aggressive malignant bone sarcoma worldwide. A causal gene network with specific functions underlying both the development and progression of OS was still unclear. Here we firstly identified the differentially expressed genes (DEGs) between control and OS samples, and then defined the hub genes and top clusters in the protein-protein interaction (PPI) network of these DEGs. By focusing on the hub gene TYROBP in the top 1 cluster, a conserved TYROBP co-expression network was identified. Then the effect of the network on OS overall survival was analyzed. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses and Gene Set Enrichment Analysis (GSEA) were used to explore the functions of the network. XCell platform and ssGSEA algorithm were conducted to estimate the status of immune infiltration. ChEA3 platform, GSEA enrichment analysis, and Drug Pair Seeker (DPS) were used to predict the key transcription factor and its upstream signal. We identified the downregulated SPI1-TYROBP-FCER1G network in OS, which were significantly enriched in immune-related functions. We also defined a two-gene signature (SPI1/FCER1G) that can predict poorer OS overall survival and the attenuated immune infiltration when downregulated. The SPI1-TYROBP-FCER1G network were potentially initiated by transcription factor SPI1 and would lead to the upregulated CD86, MHC-II, CCL4/CXCL10/CX3CL1 and hence increased immune infiltrations. With this study, we could better explore the mechanism of OS oncogenesis and metastasis for developing new therapies.

摘要

骨肉瘤是一种具有侵袭性的恶性骨肉瘤，在全球范围内普遍存在。骨肉瘤发生和进展的特定功能的因果基因网络仍不清楚。在这里，我们首先鉴定了对照和骨肉瘤样本之间的差异表达基因（DEGs），然后定义了这些 DEGs 蛋白-蛋白相互作用（PPI）网络中的枢纽基因和顶级簇。通过关注顶级簇 1 中的枢纽基因 TYROBP，确定了一个保守的 TYROBP 共表达网络。然后分析了该网络对骨肉瘤总体生存率的影响。基因本体论（GO）、京都基因与基因组百科全书（KEGG）富集分析和基因集富集分析（GSEA）用于探索网络的功能。XCell 平台和 ssGSEA 算法用于估计免疫浸润状态。ChEA3 平台、GSEA 富集分析和 Drug Pair Seeker（DPS）用于预测关键转录因子及其上游信号。我们鉴定了骨肉瘤中下调的 SPI1-TYROBP-FCER1G 网络，该网络在免疫相关功能中显著富集。我们还定义了一个可以预测骨肉瘤总体生存率较差和免疫浸润减弱的双基因特征（SPI1/FCER1G）。SPI1-TYROBP-FCER1G 网络可能由转录因子 SPI1 启动，并导致 CD86、MHC-II、CCL4/CXCL10/CX3CL1 的上调，从而增加免疫浸润。通过这项研究，我们可以更好地探索骨肉瘤发生和转移的机制，为开发新的治疗方法提供依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f24b/8790913/6698796a08e2/12885_2022_9216_Fig8_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f24b/8790913/6698796a08e2/12885_2022_9216_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f24b/8790913/c3c16b26bade/12885_2022_9216_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f24b/8790913/de4565c37ea7/12885_2022_9216_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f24b/8790913/8a8d6024f95d/12885_2022_9216_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f24b/8790913/8c4165dff96e/12885_2022_9216_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f24b/8790913/809b8fa81226/12885_2022_9216_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f24b/8790913/4f708f3f90c2/12885_2022_9216_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f24b/8790913/6698796a08e2/12885_2022_9216_Fig8_HTML.jpg

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