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基于加权基因共表达网络分析鉴定 FCER1G 为多发性骨髓瘤的关键基因。

Identification of FCER1G as a key gene in multiple myeloma based on weighted gene co-expression network analysis.

机构信息

Department of Hematology, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University; The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, People's Republic of China.

出版信息

Hematology. 2023 Dec;28(1):2210904. doi: 10.1080/16078454.2023.2210904.

Abstract

PURPOSE

Although the prognosis of multiple myeloma (MM) has remarkably improved with the emerge of novel agents, it remains incurable and relapses inevitably. The molecular mechanisms of MM have not been well-studied. Herein, this study aimed to identify key genes in MM.

MATERIALS AND METHODS

The GSE39754 dataset was used to screen differentially expressed genes (DEGs) and construct a co-expression network. Hub nodes were identified in the protein and protein interaction (PPI) network. Datasets GSE13591 and GSE2658 were used to validate hub genes. Moreover, function and gene set enrichment analyses were performed to elucidate the molecular pathogenesis of MM.

RESULTS

In this study, 11 genes were found to be hub genes in the co-expression network, among which four genes (CD68, FCER1G, PLAUR and LCP2) were also identified as hub nodes. In the test dataset GSE13591, CD68 and FCER1G were significantly downregulated in MM. Besides, the areas under the curve (AUCs) of CD68 and FCER1G were greater than 0.8 in both the training dataset and the test dataset. Our results also confirmed that FCER1G highly expressed patients had remarkably longer survival times in MM. Function and pathway enrichment analyses suggested that hub genes were associated with epithelial mesenchymal transition, TNF-α signaling via NF-κB and inflammatory response. GSEA in our study indicated that FCER1G participated in NK cell mediated cytotoxicity and the NOD-like receptor signaling pathway.

CONCLUSION

Our study identified FCER1G as a key gene in MM, providing a novel biomarker and potential molecular mechanisms of MM for further studies.

摘要

目的

尽管新型药物的出现显著改善了多发性骨髓瘤(MM)的预后,但该病仍无法治愈,且必然会复发。MM 的分子机制尚未得到充分研究。本研究旨在鉴定 MM 中的关键基因。

材料和方法

使用 GSE39754 数据集筛选差异表达基因(DEGs)并构建共表达网络。在蛋白质-蛋白质相互作用(PPI)网络中确定关键节点。使用数据集 GSE13591 和 GSE2658 验证关键基因。此外,还进行了功能和基因集富集分析,以阐明 MM 的分子发病机制。

结果

在本研究中,在共表达网络中发现了 11 个关键基因,其中 4 个基因(CD68、FCER1G、PLAUR 和 LCP2)也被鉴定为关键节点。在测试数据集 GSE13591 中,MM 中 CD68 和 FCER1G 表达显著下调。此外,CD68 和 FCER1G 的曲线下面积(AUC)在训练数据集和测试数据集均大于 0.8。我们的结果还证实,FCER1G 高表达的患者在 MM 中具有更长的生存时间。功能和通路富集分析表明,关键基因与上皮间质转化、TNF-α 信号通过 NF-κB 和炎症反应有关。本研究中的 GSEA 表明,FCER1G 参与 NK 细胞介导的细胞毒性和 NOD 样受体信号通路。

结论

本研究鉴定了 FCER1G 作为 MM 的关键基因,为进一步研究提供了新的生物标志物和 MM 的潜在分子机制。

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