期刊文献+

基于生物信息学miR-221调控前列腺癌分子机制的研究

Study on the Molecular Mechanism of Prostate Cancer Regulated by Bioinformatics miR-221
下载PDF
导出
摘要 目的:基于GEO数据库对miR-221调控前列腺癌差异基因进行分析,以期找到miR-221调控前列腺癌的重要靶点基因。方法:在GEO数据库里,获得miR-221调控前列腺癌差异基因表达的芯片GSE45627,用在线分析工具GEO2R进行数据分析,按照P<0.01和差异倍数≥2进行筛选,将筛选得到的基因输入DAVID数据库进行基因和通路的富集分析,然后进行蛋白质互做分析。结果:共鉴定108个DEG。基因本体富集结果表明,DEG编码的功能分子主要位于细胞质、细胞核,分子功能主要涉及“双链RNA结合”“螺旋酶活性”“双链DNA结合”“蛋白结合”“单链RNA结合”,与生物学过程有关,包括“调节Ⅰ型干扰素信号通路”“病毒的防御反应”“调控病毒遗传物质的复制”“先天免疫反应”。KEGG信号通路分析主要涉及甲型H1N1流感信号通路、麻疹信号通路、丙型肝炎信号通路、RIG-I样受体信号通路、Toll样受体信号通路等。结论:生物信息分析的结果可以发现miR-221调控前列腺癌中有用的靶点和信号通路,但这些需要进一步的实验验证。 Objective:To analyze the differential genes regulated by miR-221 in prostate cancer based on GEO database in order to find an important target gene for miR-221 regulation of prostate cancer.Methods:In GEO database,the chip GSE45627,which was obtained by miR-221 regulating differential gene expression in prostate cancer,was analyzed by online analysis tool GEO2R.According to P<0.01and difference multiple≥2,the obtained genes were input into DAVID database for gene and pathway enrichment analysis,and then protein interaction analysis and module analysis were carried out.The analysis results are compared with those of text mining.Results:A total of 108 DEG were identified.The results of gene ontology enrichment showed that the functional molecules encoded by DEG were mainly located in cytoplasm,nucleus,and their molecular functions were mainly related to“double-stranded RNA binding”“spiroenzyme activity”“double-stranded DNA binding”“protein binding”and“single-stranded RNA binding”,which were related to biological processes,including“regulating typeⅠinterferon signaling pathway”“defensive response to virus”and“negative regulation of viral genome replication”.KEGG signal pathway analysis mainly involves A H1N1 influenza signal pathway,measles signal pathway,hepatitis C signal pathway,RIG-I like receptor signal pathway,Toll-like receptor signal pathway and so on.Conclusion:The results of bioinformation analysis can find useful targets and signaling pathways in the regulation of prostate cancer by miR-221,but these need to be further verified by experiments.
作者 张世昌 郑江 ZHANG Shichang;ZHENG Jiang(The First Affiliated Hospital of Yangtze University,Jingzhou City,Hubei Province 434000)
出处 《医学理论与实践》 2020年第5期703-707,共5页 The Journal of Medical Theory and Practice
关键词 前列腺癌 MIR-221 生物信息学 差异基因 基因富集分析 Prostate cancer miR-221 Bioinformatics Differential gene Gene enrichment analysis
  • 相关文献

参考文献4

二级参考文献52

  • 1李学松,梁云燕,王代树,牛亦农,周利群,薛兆英,那彦群,郭应禄.中药紫龙金对前列腺癌细胞体外增殖和侵袭的抑制作用[J].中国中西医结合杂志,2005,25(S1):116-119. 被引量:7
  • 2李学松,梁云燕,王代树,谢贤和,师长进,陈捷,孙国锋,周利群,薛兆英,那彦群,郭应禄.复方中药紫龙金对前列腺癌细胞系LNCaP的体外作用[J].中国中西医结合杂志,2004,24(7):621-624. 被引量:8
  • 3刘勇,赵芳芳,夏佩莹.p^(16)和bcl-2基因与结核分枝杆菌L型感染在前列腺癌中的表达及意义[J].实用全科医学,2005,3(5):379-380. 被引量:2
  • 4张秉鸿,郭旻,王庆堂,王亮,南勋义.中药鸦胆子对前列腺癌细胞超微结构及PSA水平的影响[J].西南国防医药,2007,17(4):402-404. 被引量:8
  • 5CHIANG A C, MASSAGUE J. Molecular basis of metastasis [ J ] . N Engl J Med, 2008, 359(26): 2814-2823.
  • 6ENGSTROM C A. Hot flashes in prostate cancer: state of the sci [ J ]. Am J Mens Health, 2008, 2(2): 122-132.
  • 7FITZPATRICK J M, SCHULMAN C, ZLOTTA A R, et al. Prostate cancer: a serious disease suitable for prevention [ J ]. BJU Int, 2009, 103(7): 864-870.
  • 8JENAL M, BRITSCHGI C, FEY M F, et al. Inactivation of the hypermethylated in cancer 1 tumour suppressor--not just a question of promoter hypermethylation? [ J] Swiss Med Wkly, 2010, 140: w13106.
  • 9SAITO K, SAKURAI S, SANO T, et al. Aherrant methylatiou status of known methylation-sensitive CpG islands in gastrointestinal stromal tumors without any correlation to the state of c-kit and PDGFRA gene mutations and their malignancy [ J ]. Cancer Sei, 2008, 99(2): 253-259.
  • 10DUMONT N, WILSON M B, CRAWFORD Y G, et al. Sustained induction of epithelial to mesenehymal transition activates DNA methylation of genes silenced in basal- like breast cancers [ J ] . Proc Natl Aead Sci U S A, 2008, 105(39): 14867-14872.

共引文献20

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部