Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.molonc.2016.05.006
Title: Global re-wiring of p53 transcription regulation by the hepatitis B virus X protein
Authors: Chan, Cheryl
Thurnherr, Thomas
Wang, Jingbo 
Gallart-Palau, Xavier
Sze, Siu Kwan 
Rozen, Steve
Lee, Caroline G 
Keywords: Science & Technology
Life Sciences & Biomedicine
Oncology
P53 transcription
HBx
ChIP-Seq
Phosphorylation
p53 serine 315
CELL-CYCLE ARREST
DNA-BINDING
GENE-EXPRESSION
IN-VIVO
GENOME
SITES
TRANSACTIVATION
ACETYLATION
ASSOCIATION
INHIBITION
Issue Date: 1-Oct-2016
Publisher: WILEY
Citation: Chan, Cheryl, Thurnherr, Thomas, Wang, Jingbo, Gallart-Palau, Xavier, Sze, Siu Kwan, Rozen, Steve, Lee, Caroline G (2016-10-01). Global re-wiring of p53 transcription regulation by the hepatitis B virus X protein. MOLECULAR ONCOLOGY 10 (8) : 1183-1195. ScholarBank@NUS Repository. https://doi.org/10.1016/j.molonc.2016.05.006
Abstract: Background The tumour suppressor p53 is a central player in transcription regulation and cell fate determination. By interacting with p53 and altering its sequence-specific binding to the response elements, the hepatitis B virus X protein (HBx) was reported to re-direct p53 regulation of some genes. Results Coupling massively parallel deep sequencing with p53 chromatin immunoprecipitation, we demonstrate that HBx modulates global p53 site selection and that this was strongly influenced by altered interaction with transcription co-factors/co-regulators as well as post-translational modifications. Specifically, HBx attenuated p53-TBP-RB1 transcription complex recruitment and interaction and this was associated with hyper-phosphorylation of p53 at serine 315 by HBx. Concurrently, HBx enhanced p53 DNA occupancy to other response elements either alone by displacing specific transcription factors such as CEBPB and NFkB1, or in complex with distinct interacting co-factors Sp1, JUN and E2F1. Importantly, re-wiring of p53 transcription regulation by HBx was linked to the deregulation of genes involved in cell proliferation and death, suggesting a role of HBx in errant cell fate determination mediated by altered p53 site selection of target genes. Conclusions Our study thus presents first evidence of global modes of p53 transcription alteration by HBx and provides new insights to understand and potentially curtail the viral oncoprotein.
Source Title: MOLECULAR ONCOLOGY
URI: https://scholarbank.nus.edu.sg/handle/10635/226882
ISSN: 1878-0261
DOI: 10.1016/j.molonc.2016.05.006
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