The polyoma virus large T binding protein p150 is a transcriptional repressor of c-MYC.

The polyoma virus large T binding protein p150 is a transcriptional repressor of c-MYC.
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DOI:
10.1371/journal.pone.0046486
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Benjamin T
Benjamin T
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Sung CK;Yim H;Gu H;Li D;Andrews E;Duraisamy S;Li C;Drapkin R;Benjamin T

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p150是SALL 2基因的产物,是多瘤病毒大T抗原的结合伴侣和推定的肿瘤抑制因子。p150与c-MYC启动子的核酸酶超敏元件结合并抑制c-MYC转录。p150在人卵巢表面上皮细胞中的过表达导致c-MYC的表达降低,并下调至表达增加。c-MYC在卵巢癌细胞p150恢复后被抑制。依托泊苷诱导细胞凋亡导致p150募集到c-MYC启动子并抑制c-MYC。癌症基因组图谱中的数据分析显示,在四种常见的实体瘤类型中,SALL 2和c-MYC表达之间存在负相关性。
p150, product of the SALL2 gene, is a binding partner of the polyoma virus large T antigen and a putative tumor suppressor. p150 binds to the nuclease hypersensitive element of the c-MYC promoter and represses c-MYC transcription. Overexpression of p150 in human ovarian surface epithelial cells leads to decreased expression, and downregulation to increased expression, of c-MYC. c-MYC is repressed upon restoration of p150 to ovarian carcinoma cells. Induction of apoptosis by etoposide results in recruitment of p150 to the c-MYC promoter and to repression of c-MYC. Analysis of data in The Cancer Genome Atlas shows negative correlations between SALL2 and c-MYC expression in four common solid tumor types.
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