SUMO1 modification of histone H4 is involved in the pathogenesis of nodular lymphocyte predominant Hodgkin lymphoma.

SUMO1 modification of histone H4 is involved in the pathogenesis of nodular lymphocyte predominant Hodgkin lymphoma.
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组蛋白 H4 的 SUMO1 修饰参与结节性淋巴细胞为主的霍奇金淋巴瘤的发病机制

DOI:
10.21037/tcr-20-1994
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发表时间:
2020-07
影响因子:
0.9
通讯作者:
Li X
Li X
中科院分区:
医学4区
文献类型:
--
作者:
Li H;Guo L;Li B;Li X

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结节性淋巴细胞显性霍奇金淋巴瘤(NLPHL)是霍奇金淋巴瘤(HL)的一种独特而罕见的亚型,可与经典霍奇金淋巴瘤(cHL)鉴别诊断。由于其低患病率和不明确的致病机制,特异性治疗NLPHL尚未确定。NLPHL是一种恶性B细胞淋巴瘤,抗原刺激导致次级淋巴滤泡形成生发中心,促进生发中心B细胞(GCBs)分化为长寿的浆细胞和记忆B细胞。分化过程中的任何异常都可能导致NLPHL的发生和发展。GDS4977数据集选自Gene Expression Omnibus (GEO)数据库。用GEO2R检测差异表达基因(DEGs)。基因本体(GO)富集分析的生物过程(BP)和Reactome途径进行:Profile。使用Cytoscape软件筛选中心基因,使用STRING和Reactome数据库确定核心基因。共鉴定出623个deg、68个GO-BP通路、70个Reactome通路、19个枢纽基因和12个核心基因。NLPHL和GCBs的组蛋白表达不同,HIST1H4B、HIST1H4C、HIST1H4E、HIST1H4L、HIST1H2AE、H2AFZ、HIST1H2BM和H3F3A共同构成核心组蛋白。在NLPHL的发展过程中,组蛋白由NPM1运输。NLPHL的发病机制涉及组蛋白H4的SUMO-1修饰。
Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is a distinct and rare subtype of Hodgkin lymphoma (HL) that can be differentially diagnosed from classical Hodgkin lymphoma (cHL). Because of its low prevalence rate and undefined pathogenic mechanisms, a specific treatment for NLPHL has yet to be determined. In NLPHL, which is a malignant B-cell lymphoma, antigen stimulation results in the formation of germinal centers by secondary lymphoid follicles, which promotes the differentiation of germinal center B cells (GCBs) into long-lived plasma cells and memory B cells. Any abnormality during the differentiation can lead to the occurrence and development of NLPHL. The GDS4977 data set was selected from the Gene Expression Omnibus (GEO) repository. Differentially-expressed genes (DEGs) were detected with GEO2R. Gene Ontology (GO) enrichment analysis of biological processes (BP) and Reactome pathways was performed withg:Profile. Cytoscape software was employed to screen hub genes, while the core genes were determined using the STRING and Reactome databases. In total, 623 DEGs, 68 GO-BP pathways, 70 Reactome pathways, 19 hub genes, and 12 core genes were identified. Histone expressions differ between NLPHL and GCBs, and HIST1H4B, HIST1H4C, HIST1H4E, HIST1H4L, HIST1H2AE, H2AFZ, HIST1H2BM, and H3F3A jointly form the core histones. During the development of NLPHL, histones are transported by NPM1. The pathogenesis of NLPHL involves SUMO-1 modification of histone H4.
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