CAJ | 학술논문

目的筛选前列腺癌发生发展过程中的差异表达基因,构建差异调控网络.方法从基因表达数据库(GEO)中下载编号为GSE3325的基因芯片(13例正常、原发性前列腺癌和转移性前列腺癌的独立样本与6例三者的混合样本),筛选前列腺癌和正常前列腺组织的差异基因(P＜0.05及差异值＞2或＜-2)；计算差异基因与靶基因间的皮尔森相关系数(| PCC |＞0.75),构建差异调控网络；基因本体论(GO)富集方法分析差异调控网络基因的功能.结果原发性前列腺癌与正常前列腺组织筛选到5847个差异表达基因,转移性前列腺癌与正常前列腺组织筛选到2026个差异基因,原发性前列腺癌与转移性前列腺癌筛选到977个共同的差异基因；原癌基因同源体( MYC)、E2F转录因子1(E2F1)、肿瘤蛋白53( TP53)和雌激素受体1(ESR1)基因在差异调控网络中起核心作用.结论筛选出前列腺癌的差异表达基因.
목적 사선전렬선암발생발전과정중적차이표체기인,구건차이조공망락.방법 종기인표체수거고(GEO)중하재편호위GSE3325적기인심편(13례정상、원발성전렬선암화전이성전렬선암적독립양본여6례삼자적혼합양본),사선전렬선암화정상전렬선조직적차이기인(P＜0.05급차이치＞2혹＜-2)；계산차이기인여파기인간적피이삼상관계수(| PCC |＞0.75),구건차이조공망락；기인본체론(GO)부집방법분석차이조공망락기인적공능.결과 원발성전렬선암여정상전렬선조직사선도5847개차이표체기인,전이성전렬선암여정상전렬선조직사선도2026개차이기인,원발성전렬선암여전이성전렬선암사선도977개공동적차이기인；원암기인동원체( MYC)、E2F전록인자1(E2F1)、종류단백53( TP53)화자격소수체1(ESR1)기인재차이조공망락중기핵심작용.결론 사선출전렬선암적차이표체기인.
Objective To construct regulation networks using differentially expressed genes in prostate cancer screened by DNA microarray.Methods We downloaded the gene expression profile of prostate cancer from Gene Expression Omnibus database which includes 13 individual benign prostate,primary and metastatic prostate cancer samples and 6 pooled samples from benign,primary or metastatic prostate cancer tissues.We identified the differentially expressed genes (DEGs) between prostate cancer and benign prostate tissue with the threshold of P ＜ 0.05 and fold change value ＞ 2 or ＜ - 2.We calculated the Pearson Correlation Coefficient (PCC) between the DEGs and their target genes to construct regulation networks with the cut off criterion of | PCC | ＞ 0.75.GO enrichment method was used to analyze the function of genes in regulation networks.Results Total 5847 genes were identified as DEGs between primary prostate cancer and benign prostate tissue,and total 2026 genes were identified as DEGs between metastatic prostate cancer and benign prostate tissue.There were a total of 977 overlapping DEGs.Oncogene homolog ( MYC),E2F transcription factor 1 ( E2F1 ),tumor protein 53 ( TP53 ) and estrogen receptor 1 ( ESR1 )were shown as hub nodes in the regulation networks,suggesting these genes may play important roles in the progression of prostate cancer.Conclusion We identified the DEGs associated with progression of prostate cancer.Results from our study will provide the ground work for the further study on the molecular mechanism of prostate cancer.