|本期目录/Table of Contents|

[1]陈赛鹏,王嘉南,王 林,等.基于TCGA数据库分析甲基化促进精原细胞瘤进程的作用机制[J].天津医科大学学报,2019,25(05):463-465+470.
　CHEN Sai-peng,WANG Jia-nan,WANG Lin,et al.Integrated analysis of the mechanism of methylation promoting the progress of seminomas based on the TCGA database[J].Journal of Tianjin Medical University,2019,25(05):463-465+470.
点击复制

基于TCGA数据库分析甲基化促进精原细胞瘤进程的作用机制(PDF)
分享到：

《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
25卷
期数:
2019年05期
页码:
463-465+470
栏目:
基础医学
出版日期:
2019-09-20

文章信息/Info

Title:
Integrated analysis of the mechanism of methylation promoting the progress of seminomas based on the TCGA database
文章编号:
1006-8147(2019)05-0463-03
作者:
陈赛鹏; 王嘉南; 王 林; 彭华红; 肖龙飞; 杨 阔
（天津医科大学第二医院泌尿外科，天津市泌尿外科研究所，天津 300211）
Author(s):
CHEN Sai-peng;  WANG Jia-nan;  WANG Lin;  PENG Hua-hong;  XIAO Long-fei;  YANG Kuo
（Department of Urology, The Second Hospital, Tianjin Medical University, Tianjin Institute of Urology, Tianjin 300211, China）
关键词:
精原细胞瘤; 甲基化; TCGA数据库; KCNC1
Keywords:
iminomas;  methylation;  TCGA;  KCNC1
分类号:
R737
DOI:
-
文献标志码:
A
摘要:
目的：通过生物信息学分析寻找甲基化促进精原细胞瘤进展的作用机制。方法：获取TCGA数据库精原细胞瘤数据，对Ⅱ期、Ⅲ期和Ⅰ期样本之间的差异甲基化位点、差异基因进行查找和关联分析，筛选精原细胞瘤Ⅱ期、Ⅲ期和Ⅰ期之间可能通过甲基化导致基因改变并影响精原细胞瘤的潜在机制。结果：分析显示KCNC1的表达与甲基化呈显著负相关，并显著影响精原细胞瘤患者的生存期。结论：利用生物信息学技术对不同分期的精原细胞瘤芯片数据分析，可发现高甲基化水平会导致基因KCNC1低表达，进而促进精原细胞瘤的进展，为靶向治疗精原细胞瘤提供精确方向。
Abstract:
Objective: To explore the mechanism of methylation promoting the development of seminomas. Methods: Transcriptome sequencing data of seminomas patients from TCGA database were downloaded, correlation analysis of the differential methylation probs and differential genes of stage Ⅱ/Ⅲ and Ⅰ periods seminomas was carried. The mechanism by which methylation may lead to changes in gene expression and affect the progress of seminomas was analyzed. Results: Analysis showed that the expression of KCNC1 was negatively correlated with methylation and significantly affected the survival of patients with seminoma.Conclusion: Using bioinformatics technology to analyze the microarray data of siminomas in different stages, it we have found that high methylation level may lead to low expression of gene KCNC1, thus promoting the progress of siminomas and providing support for targeted treatment of siminomas.

参考文献/References:

[1] Gonzalez-Exposito R, Merino M, Aguayo C. Molecular biology of testicular germ cell tumors[J]. Clin Transl Oncol, 2016,18(6):550
[2] Di Pietro A, Vries E G, Gietema J A, et al. Testicular germ cell tumours: the paradigm of chemo-sensitive solid tumours[J]. Int J Biochem Cell B, 2005, 37(12):2437
[3] Richie J P. Re: Management of seminomatous testicular cancer: A binational prospective population-based study from the swedish norwegian testicular cancer study group[J]. J Urology,2011, 186(6):2255
[4] Chung P W, Gospodarowicz M K, Panzarella T J, et al. Stage II testicular seminoma: patterns of recurrence and outcome of treatment[J]. Eur Urol, 2004, 45(6):754
[5] Bird A. DNA methylation patterns and epigenetic memory[J]. Gene Dev, 2002, 16(1):6
[6] Costello J F, Plass C. Methylation matters[J]. J Med Genet, 2001,38(5):285
[7] Rapley E A, Turnbull C, Al Olama A A, et al. A genome-wide association study of testicular germ cell tumor[J]. Nat Genet, 2009,41(7):807
[8] Kanetsky P A, Mitra N, Vardhanabhuti S, et al. A second independent locus within DMRT1 is associated with testicular germ cell tumor susceptibility[J]. Hum Mol Genet,2011,20(15):3109
[9] Kratz C P, Greene M H, Bratslavsky G, et al. A stratified genetic risk assessment for testicular cancer[J]. Int J Androl, 2011,34(4 Pt 2):e98
[10] Kanetsky P A, Mitra N, Vardhanabhuti S, et al. Common variation in KITLG and at 5q31.3 predisposes to testicular germ cell cancer[J]. Nat Genet,2009,41(7):811
[11] Karlsson R, Andreassen K E, Kristiansen W, et al. Investigation of six testicular germ cell tumor susceptibility genes suggests a parent-of-origin effect in SPRY4[J]. Hum Mol Genet, 2013,22(16):3373
[12] Ruark E, Seal S, McDonald H, et al. Identification of nine new susceptibility loci for testicular cancer, including variants near DAZL and PRDM14[J]. Nat Genet, 2013,45(6):686
[13] Akhavan-Niaki H, Samadani A A. DNA methylation and cancer development: molecular mechanism[J]. Cell Biochem Bioph, 2013, 67(2):501
[14] Perney T M, Marshall J, Martin K A, et al.Expression of the mRNAs for the Kv3.1 potassium channel gene in the adult and developing rat brain[J]. J Neurophysiol, 1992,68(3):756
[15] Stegen B, Klumpp L, Misovic M E, et al. K(+) channel signaling in irradiated tumor cells[J]. Eur Biophys J Bioph, 2016,45(7):585
[16] Edalat L, Stegen B, Klumpp L, et al. BK K+ channel blockade inhibits radiation-induced migration/brain infiltration of glioblastoma cells[J]. Oncotarget, 2016,7(12):14259
[17] Ouadid-Ahidouch H, Ahidouch A. K+ channel expression in human breast cancer cells: involvement in cell cycle regulation and carcinogenesis[J]. J Membrane Biol, 2008,221(1):1

相似文献/References:

[1]郭小凡 综述,邓靖宇,梁 寒 审校.PCDH10启动子甲基化与恶性肿瘤关系的研究进展[J].天津医科大学学报,2016,22(02):182.
[2]史 艺,姚爱琳,张爱华.睾丸女性化综合征合并精原细胞瘤1例报道[J].天津医科大学学报,2016,22(06):497.
[3]闫墨,刘帅兵,王楷斌,等.基于生物信息学方法筛选精原细胞瘤进展中的脂代谢关键基因[J].天津医科大学学报,2022,28(06):585.
　YAN Mo,LIU Shuai-bing,WANG Kai-bin,et al.Identification of key lipid metabolism genes in the progress of seminoma by integrated bioinformatics analysis[J].Journal of Tianjin Medical University,2022,28(05):585.
[4]张静怡,迟航,杨鑫,等.Ras相关区域家族10蛋白在非小细胞肺癌中的表达及预后价值[J].天津医科大学学报,2024,30(05):385.[doi:10.20135/j.issn.1006-8147.2024.05.0385]
　ZHANG Jingyi,CHI Hang,YANG Xin,et al.The expression and prognostic value of ras-association domain family 10 in non-small cell lung cancer[J].Journal of Tianjin Medical University,2024,30(05):385.[doi:10.20135/j.issn.1006-8147.2024.05.0385]

备注/Memo

备注/Memo:
作者简介 陈赛鹏（1991-），男，硕士在读，研究方向：泌尿外科；通信作者：杨阔，E-mail：ykuoster@126.com。
更新日期/Last Update: 2019-10-11