The Polyoma Virus Large T Binding Protein p150 Is a Transcriptional Repressor of c-MYCopen access
- Authors
- Sung, C.K.; Yim, H.; Gu, H.; Li, D.; Andrews, E.; Duraisamy, S.; Li, C.; Drapkin, R.; Benjamin, T.
- Issue Date
- Sep-2012
- Keywords
- unclassified drug; transcription regulation; Antineoplastic Agents, Phytogenic; protein p 150; Proto-Oncogene Proteins c-myc; Humans; epithelium cell; Gene Expression Regulation, Neoplastic; solid tumor; Molecular Sequence Data; apoptosis; Myc protein; ca
- Citation
- PLoS ONE, v.7, no.9, pp.1 - 7
- Indexed
- SCIE
SCOPUS
- Journal Title
- PLoS ONE
- Volume
- 7
- Number
- 9
- Start Page
- 1
- End Page
- 7
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/36226
- DOI
- 10.1371/journal.pone.0046486
- ISSN
- 1932-6203
- Abstract
- 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. © 2012 Sung et al.
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