生物技术通讯
生物技術通訊
생물기술통신
LETTERS IN BIOTECHNOLOGY
2013年
1期
104-108
,共5页
垂体瘤转化基因1%靶基因%肝癌
垂體瘤轉化基因1%靶基因%肝癌
수체류전화기인1%파기인%간암
pituitary tumor-transforming gene-1%target genes%hepatocellular carcinoma
垂体瘤转化基因1(PTTG1),也被称为分离酶抑制蛋白基因,是近几年从大鼠垂体肿瘤中发现的癌基因.它不但可以与分离酶结合,使分离酶失活,从而抑制姐妹染色单体的分离,还具有转录激活活性.已有的染色质免疫共沉淀结合芯片数据显示,PTTG1不仅可以直接调控基因的转录,也可以与其他蛋白,如PTTG1结合因子(PBF)、p53、Sp1、上游刺激因子1(USF1)等相互作用来调控下游基因的转录.在NIH 3T3细胞中,PTTG1激活c-Myc的转录,增强NIH 3T3细胞在裸鼠体内的成瘤能力.PTTG1也能激活肿瘤细胞中成纤维细胞生长因子2(FGF2)的转录,从而促进肿瘤血管生成.PTTG1结合p53、抑制p21表达、激活周期蛋白D3的能力,提示它在凋亡、细胞周期和衰老方面也发挥作用.另外,PTTG1在肿瘤转移和肝癌的发生发展中也发挥着重要作用.我们简要综述了PTTG1的靶基因,及其在肝癌及肿瘤转移中的研究进展.
垂體瘤轉化基因1(PTTG1),也被稱為分離酶抑製蛋白基因,是近幾年從大鼠垂體腫瘤中髮現的癌基因.它不但可以與分離酶結閤,使分離酶失活,從而抑製姐妹染色單體的分離,還具有轉錄激活活性.已有的染色質免疫共沉澱結閤芯片數據顯示,PTTG1不僅可以直接調控基因的轉錄,也可以與其他蛋白,如PTTG1結閤因子(PBF)、p53、Sp1、上遊刺激因子1(USF1)等相互作用來調控下遊基因的轉錄.在NIH 3T3細胞中,PTTG1激活c-Myc的轉錄,增彊NIH 3T3細胞在裸鼠體內的成瘤能力.PTTG1也能激活腫瘤細胞中成纖維細胞生長因子2(FGF2)的轉錄,從而促進腫瘤血管生成.PTTG1結閤p53、抑製p21錶達、激活週期蛋白D3的能力,提示它在凋亡、細胞週期和衰老方麵也髮揮作用.另外,PTTG1在腫瘤轉移和肝癌的髮生髮展中也髮揮著重要作用.我們簡要綜述瞭PTTG1的靶基因,及其在肝癌及腫瘤轉移中的研究進展.
수체류전화기인1(PTTG1),야피칭위분리매억제단백기인,시근궤년종대서수체종류중발현적암기인.타불단가이여분리매결합,사분리매실활,종이억제저매염색단체적분리,환구유전록격활활성.이유적염색질면역공침정결합심편수거현시,PTTG1불부가이직접조공기인적전록,야가이여기타단백,여PTTG1결합인자(PBF)、p53、Sp1、상유자격인자1(USF1)등상호작용래조공하유기인적전록.재NIH 3T3세포중,PTTG1격활c-Myc적전록,증강NIH 3T3세포재라서체내적성류능력.PTTG1야능격활종류세포중성섬유세포생장인자2(FGF2)적전록,종이촉진종류혈관생성.PTTG1결합p53、억제p21표체、격활주기단백D3적능력,제시타재조망、세포주기화쇠로방면야발휘작용.령외,PTTG1재종류전이화간암적발생발전중야발휘착중요작용.아문간요종술료PTTG1적파기인,급기재간암급종류전이중적연구진전.
Pituitary tumor-transforming gene-1(PTTG1), also named securin, is a transforming gene first discov?ered in rat pituitary tumor cells. Not only dose it have securin functions, but also possesses transcriptional activi?ty. Chromatin immunoprecipitation-on-chip(ChIP-on-chip) study revealed that PTTG1 is a global transcription fac?tor, which exerts its transcriptional activity either by directly binding to DNA or by interacting with other known transcription factors including PTTG1 binding factor(PBF), p53, Sp1, and upstream stimulatory factor 1(USF1). PTTG1 has several validated transcriptional targets that are involved in diverse cellular processes. PTTG1 activates c-Myc in NIH 3T3 cells, suggesting a role in cell transformation. PTTG1 induces the expression of fibroblast growth factor 2(FGF2) and promotes tumor angiogenesis. It binds to and inhibits p53 transcriptional activity. PTTG1 activates cyclin D3 and represses p21 expression, indicating a role in cell cycle regulation and cell senes?cence. Hence, we reviewed PTTG1 and its transcriptional targets, and discussed their implications in tumor devel?opment and metastasis, especially in the context of hepatocellular carcinoma.