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  4. Breast cancer amplified sequence 2, a novel negative regulator of the p53 tumor suppressor
 
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Breast cancer amplified sequence 2, a novel negative regulator of the p53 tumor suppressor

Journal
Cancer Research
Journal Volume
69
Journal Issue
23
Pages
8877-8885
Date Issued
2009
Author(s)
Kuo P.-C.
Tsao Y.-P.
Chang H.-W.
Chen P.-H.
Huang C.-W.
Lin S.-T.
Weng Y.-T.
Tsai T.-C.
Shieh S.-Y.
SHOW-LI CHEN  
DOI
10.1158/0008-5472.CAN-09-2023
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-71549159140&doi=10.1158%2f0008-5472.CAN-09-2023&partnerID=40&md5=09d8de55cc4306d91d425397ad0b6dbf
https://scholars.lib.ntu.edu.tw/handle/123456789/416938
Abstract
Breast cancer amplified sequence 2 (BCAS2) was reported previously as a transcriptional coactivator of estrogen receptor. Here, we report that BCAS2 directly interacts with p53 to reduce p53 transcriptional activity by mildly but consistently decreasing p53 protein in the absence of DNA damage. However, in the presence of DNA damage, BCAS2 prominently reduces p53 protein and provides protection against chemotherapeutic agent such as doxorubicin. Deprivation of BCAS2 induces apoptosis in p53 wild-type cells but causes G2-M arrest in p53-null or p53 mutant cells. There are at least two apoptosis mechanisms induced by silencing BCAS2 in wildtype p53-containing cells. Firstly, it increases p53 retention in nucleus that triggers the expression of apoptosis-related genes. Secondly, it increases p53 transcriptional activity by raising p53 phosphorylation at Ser46 and decreases p53 protein degradation by reducing p53 phosphorylation at Ser315. We show for the first time that BCAS2, a small nuclear protein (26 kDa), is a novel negative regulator of p53 and hence a potential molecular target for cancer therapy. ?2009 American Association for Cancer Research.
SDGs

[SDGs]SDG3

Other Subjects
breast cancer amplified sequence 2 protein; DNA; doxorubicin; nuclear protein; protein p53; serine derivative; unclassified drug; apoptosis; article; cancer therapy; cell growth; controlled study; DNA damage; gene expression; gene overexpression; gene silencing; genetic transcription; growth inhibition; human; human cell; priority journal; protein degradation; protein phosphorylation; protein protein interaction; protein targeting; transcription initiation; tumor suppressor gene; wild type; Apoptosis; Breast Neoplasms; Cell Growth Processes; Cell Line, Tumor; Cell Nucleus; DNA Damage; Humans; Neoplasm Proteins; Protein Binding; Protein Processing, Post-Translational; Protein Structure, Tertiary; Transcriptional Activation; Tumor Suppressor Protein p53
Type
journal article

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