中华肿瘤杂志
中華腫瘤雜誌
중화종류잡지
CHINESE JOURNAL OF ONCOLOGY
2009年
8期
561-565
,共5页
刘冉录%徐勇%张志宏%王萌%孙建涛%张玥%李胜芝
劉冉錄%徐勇%張誌宏%王萌%孫建濤%張玥%李勝芝
류염록%서용%장지굉%왕맹%손건도%장모%리성지
核干因子%前列腺肿瘤%基因芯片
覈榦因子%前列腺腫瘤%基因芯片
핵간인자%전렬선종류%기인심편
Nucleostemin%Prostate neoplasms%Gene chips
目的 探讨核干因子(NS)基因在前列腺癌恶性增殖中的作用机制.方法 采用表达谱基因芯片技术,分析前列腺癌PC-3细胞NS基因表达下调后全基因组表达谱的变化,筛选与NS相互作用的差异表达基因及信号通路.采用实时荧光定量聚合酶链反应对重要的差异表达基因进行验证.结果 共筛选出219个差异表达的基因,这些基因涉及到细胞周期、细胞增殖、信号转导、细胞凋亡和细胞分化等多个方面.NS基因表达下调后主要引起周期素依赖激酶4抑制因子(INK4)家族基因(p15、p16和p18)的上调,以及cyclin D1和HDACI基因的下调,其主要作用点位于CDK4/6-cyclinD和pRb-E2F1复合体上.结论 在前列腺癌PC-3细胞中,NS基因可能主要通过抑制p15、p16和p18等INK4家族的肿瘤抑制基因的表达,从而促进肿瘤的发生和发展;NS基因是细胞周期G1/S期检查点的重要调控因子.
目的 探討覈榦因子(NS)基因在前列腺癌噁性增殖中的作用機製.方法 採用錶達譜基因芯片技術,分析前列腺癌PC-3細胞NS基因錶達下調後全基因組錶達譜的變化,篩選與NS相互作用的差異錶達基因及信號通路.採用實時熒光定量聚閤酶鏈反應對重要的差異錶達基因進行驗證.結果 共篩選齣219箇差異錶達的基因,這些基因涉及到細胞週期、細胞增殖、信號轉導、細胞凋亡和細胞分化等多箇方麵.NS基因錶達下調後主要引起週期素依賴激酶4抑製因子(INK4)傢族基因(p15、p16和p18)的上調,以及cyclin D1和HDACI基因的下調,其主要作用點位于CDK4/6-cyclinD和pRb-E2F1複閤體上.結論 在前列腺癌PC-3細胞中,NS基因可能主要通過抑製p15、p16和p18等INK4傢族的腫瘤抑製基因的錶達,從而促進腫瘤的髮生和髮展;NS基因是細胞週期G1/S期檢查點的重要調控因子.
목적 탐토핵간인자(NS)기인재전렬선암악성증식중적작용궤제.방법 채용표체보기인심편기술,분석전렬선암PC-3세포NS기인표체하조후전기인조표체보적변화,사선여NS상호작용적차이표체기인급신호통로.채용실시형광정량취합매련반응대중요적차이표체기인진행험증.결과 공사선출219개차이표체적기인,저사기인섭급도세포주기、세포증식、신호전도、세포조망화세포분화등다개방면.NS기인표체하조후주요인기주기소의뢰격매4억제인자(INK4)가족기인(p15、p16화p18)적상조,이급cyclin D1화HDACI기인적하조,기주요작용점위우CDK4/6-cyclinD화pRb-E2F1복합체상.결론 재전렬선암PC-3세포중,NS기인가능주요통과억제p15、p16화p18등INK4가족적종류억제기인적표체,종이촉진종류적발생화발전;NS기인시세포주기G1/S기검사점적중요조공인자.
Objective To screen the genes and possible signal transduction pathways involved in the mechanism of nucleostemin (NS) in the proliferation of prostate cancer. Methods Oligonucleotide DNA microarray was used to screen the genome changes after knocking-down expression of NS in PC-3 cells and quantitative real-time PCR was used to further confirm the important differentially expressed genes. Results 219 differentially expressed genes were found and theses genes were involved in cell cycle, cell proliferation, signal transduction, cell apoptosis and cell differentiation, etc. INK4 family genes (p15, p16, p18) were up-regulated and cyclin D1, HDAC1 were down-regulated, the main action points were CDK4/6-cyclin D and pRb-E2FI complexes. Conclusion NS may promote the progression of prostate cancer by inhibiting the expression of p15, p16, and p18 in PC-3 cells. NS is an important G1/S checkpoint regulator and its regulatory activity has been certified at gene level.