基于生物信息学方法的人类GLTP在胰腺腺癌发生发展中的作用及其表观遗传调控机制分析

Analysis of the Role of Human GLTP in the Initiation and Progression of Pancreatic Adenocarcinoma and Its Epigenetic Regulation Mechanisms Based on Bioinformatics Methods

通过生物信息学方法分析人类糖脂转运蛋白(GLTP)的基因在肿瘤发生发展中的作用及其表观遗传调控机制。利用UCSC Genome Browser、EMBOSS及GEPIA等在线生物信息学分析工具分析人类GLTP在肿瘤组织中的表达及生存,结果表明人类GLTP在胰腺腺癌(PAAD)组织中的表达水平显著高于癌旁正常组织,提示GLTP很可能参与了PAAD的发生发展。GLTP表达水平与PAAD患者病理分期的分析结果表明,GLTP表达水平在PAAD患者不同病理分期中的差异不显著。甲基化分析结果表明,在PAAD细胞中,人类GLTP的甲基化程度与GLTP的表达水平显著相关。组蛋白修饰分析的结果表明,组蛋白H3K4Me1、H3K27Ac可能通过上调人类GLTP的表达进而影响肿瘤的发生发展进程。内源竞争RNA(ceRNA)调控分析结果表明,人类GLTP与多种microRNA(miRNA)有潜在作用,并且这些miRNA与多种肿瘤及信号通路存在较强的关联性。本研究的结果为进一步研究人类GLTP的功能及其表观遗传调控机制提供了参考。

The role of human glycolipid transfer protein(GLTP)in initiation and progression of tumor and its epigenetic regu-lation mechanisms were analyzed by bioinformatics methods.The expression and survival analysis results of human GLTP in pancreatic adenocarcinoma(PAAD)tissues was significantly higher than that in adjacent normal tissues by using online bioin-formatics analysis tools such as UCSC Genome Browser,EMBOSS and GEPIA.These results suggest that GLTP may be in-volved in the initiation and progression of PAAD.The analysis of GLTP expression level and pathological stage of PAAD pa-tients showed that there was no significant difference in GLTP expression level among different pathological stages of PAAD patients.The results of methylation analysis showed that the methylation level of human GLTP was significantly correlated with the expression level of GLTP in PAAD cells.The results of histone modification analysis indicate that histone H3K4Me1 and H3K27Ac may affect initiation and progression of tumor by up-regulating the expression of human GLTP.The results of competing endogenous RNAs(ceRNA)regulation analysis show that human GLTP has potential effects on a variety of microRNAs(miRNAs),and these miRNAs are strongly associated with many tumors and signaling pathways.The results of this study pro-vide a reference for the further study of the function and epigenetic regulation mechanisms of human GLTP.