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甲状腺乳头状癌相关致病基因及microRNAs的筛选和生物信息学分析 被引量:1

Screening and Bioinformatics Analysis of Thyroid Papillary Carcinoma Related Genes and MicroRNAs
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摘要 本研究利用美国国家生物技术信息中心(NCBI)基因表达综合数据库(GEO)下载获取甲状腺乳头状癌(papillary thyroid carcinoma,PTC)m RNA表达谱芯片(7例PTC样本VS 7例正常组样本,登录号为GSM85-215~GSM85228)及miro RNA高通量测序数据(3例PTC样本VS 3例正常组样本,GSM1388420~GSM138-8425)。通过Qlucore Omics Explorer(QOE)3.2、DAVID 6.7、STING 9.1、mi Records等分析软件对PTC差异基因及micro RNA进行综合生物信息学分析。筛选出来497个甲状腺乳头状癌相关致病基因及86个相关micro RNAs;其中,致病基因中上调表达的有257个,下调表达的有240个;micro RNAs中上调表达的有47个,下调表达的有39个。对其进行生物信息学分析发现,ERBB3、TNNT1、MYL1、POSTN基因及hsa-mi R-183-5p(ERBB4)、hsa-mi R-139-5p(SUV39H1)、hsa-mi R-152(MAML1)、hsa-mi R-1(FOXD3)、hsa-mi R-146b-5p(MEF2C)、hsa-mi R-152(DOT1L)、hsa-mi R-493-5p(FBXW7)、hsa-mi R-876-5p(PIK3R1)、hsa-mi R-183-3p(MDM2)、hsa-mi R-382-3p(CD80)、hsa-mi R-181b-5p(SIRT1)、hsa-mi R-874-5p(MTOR)、hsa-mi R-876-5p(GPRC6A)等micro RNAs-靶基因参与涉及Erb B信号通路、细胞凋亡信号通路、B细胞受体信号通路、磷脂酰肌醇代谢信号通路等,在PTC疾病发生发展中可能起着重要作用。从分子水平上分析甲状腺乳头状癌相关致病基因及micro RNAs,为揭示PTC发病机制、药物研发及临床诊断治疗提供新的思路和依据。 In this research, we downloaded papillary thyroid carcinoma (PTC) mRNA expression profile micro- array (7 PTC samples VS 7 normal samples, accession number: GSM85215-GSM85228) and microRNA high throughput sequencing data (3 PTC samples VS 3 normal samples, accession number: GSM1388420-GSM 1388425) from NCBI and GEO. We conducted comprehensive bioinformatics analysis of PTC differential expressed genes and microRNA with Qlucore Omics Explorer (QOE) 3.2, DAVID 6.7, STING 9.1, miRecords and so on. 497 PTC related pathogenic genes and 86 microRNAs were screened out. Among them, there were 257 up-regulated genes and 240 down regulated genes in pathogenic gene, and 47 up-regulated microRNAs and 39 down regulated microRNAs. Bioinformatics analysis indicated that genes including ERBB3, TNNT1, MYL1, POSTN and microRNAs target genes including hsa-miR-183-5p (ERBB4), hsa-miR-139-5p (SUV39H1), hsa-miR-152 (MA ML1), hsa-miR-1 (FOXD3), hsa-miR-146b-5p (MEF2C), hsa-miR-152 (DOT1L), hsa-miR-493-5p (FBXW7), hsa-miR-876-5p (PIK3R1), hsa-miR-183-3p (MDM2), hsa-miR-382-3p (CD80), hsa-miR-181b-5p (SIRT1), hsa-miR-874-5p (MTOR), hsa-miR-876-5p (GPRC6A) participated in some signaling pathways, including ErbB, apoptotic, B cell receptor and phosphatidylinositol metabolism, which might play an important role in the development of PTC. We analyzed papillary thyroid carcinoma related genes and microRNAs in molecular level, which gave new thinking and evidence for pathogenesis, drug research, clinical diagnose and treatment of PTC.
作者 韩友霞 樊桂萍 季葆华 刘海燕 Han Youxia;Fan Guiping;Ji Baohua;Liu Haiyan(Beijing Institute of Technology Hospital, Beijing, 100081;Beijing Institute of Technology, Beijing, 100081)
出处 《基因组学与应用生物学》 CAS CSCD 北大核心 2017年第11期4419-4431,共13页 Genomics and Applied Biology
基金 国家自然科学基金(项目号:11372042)资助
关键词 甲状腺乳头状癌 致病基因 MICRORNAS 生物信息学分析 PTC, Pathogenic gene, Micro RNAs, Bioinformatics analysis
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  • 1Ernst P, Wang J, Korsmeyer SJ. The role of MLL in hematopoiesis and leukemia. Curr Opin Hematol, 2002 ; 9 (4) : 282 - 287.
  • 2Canaani E, Nakamura T, Rozovskaia T, et al. ALL-1/MLL1, a homologue of Drosophila TRITHORAX, modifies chromatin and is di- reetlyinvolved in infant acute leukaemia. Br J Cancer, 2004; 90 (4) : 756 -760.
  • 3Krivtsov AV, Armstrong SA. MLL translocations, histone modifica- tions and leukaemia stem-cell development. Nat Rev Cancer, 2007; 7(11) : 823 -833.
  • 4Dou Y, Hess JL. Mechanisms of transcriptional regulation by MLL and its disruption in acute leukemia. Int J Hematol, 2008 ; 87 ( 1 ) : 10 - 18.
  • 5Liedtke M, Cleary ML. Therapeutic targeting of MLL. Blood, 2009 ; 113(24) : 6061 -6068.
  • 6Nguyen AT, Zhang Y. The diverse functions of Dotl and H3K79 methylation. Genes Dev, 2011 ; 25(13) : 1345 - 1358.
  • 7Ng HH, Feng Q, Wang H, et al. Lysine methylation within the globular domain of histone H3 by Dotl is important for telomerie si- lencingand Sir protein association. Genes Dev, 2002; 16 ( 12 ) : 1518 - 1527.
  • 8van Leeuwen F, Gafken PR, Gottsehling DE. Dotlp modulates si- fencing in yeast by methylation of the nueleosome core. Cell, 2002 ; 109(6) : 745 -756.
  • 9Feng Q, Wang H, Ng HH, et al. Methylation of H3-1ysine 79 is me- diated by a new family of HMTases without a SET domain. Curr Bi- al, 2002; 12(12) : 1052 - 1058.
  • 10Lacoste N, Utley RT, Hunter JM, et al. Disruptor of telomeric silen- cing-1 is a chromatin-specific H3 methyl-transferase. J Biol Chem, 2002 ; 277 (34) : 30421 - 30424.

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