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Berscheminski, J.* ; Brun, J.* ; Speiseder, T.* ; Wimmer, P.* ; Ip, W.H.* ; Terzic, M. ; Dobner, T.* ; Schreiner, S.

Sp100A is a tumor suppressor that activates p53-dependent transcription and counteracts E1A/E1B-55K-mediated transformation.

Oncogene 35, 3178-3189 (2016)

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Open Access Green as soon as Postprint is submitted to ZB.

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Human adenoviruses (HAdV) are used as a model system to investigate tumorigenic processes in mammalian cells where the viral oncoproteins E1A and E1B-55K are absolutely required for oncogenic transformation, because they simultaneously accelerate cell cycle progression and inhibit tumor suppressor proteins such as p53, although the underlying mechanism is still not understood in detail. In our present study, we provide evidence that E1B-55K binding to the PML-NB component Sp100A apparently has an essential role in regulating adenovirus-mediated transformation processes. Specifically, when this E1B-55K/Sp100A complex recruits p53, Sp100A-induced activation of p53 transcriptional activity is effectively abolished. Hence, Sp100A exhibits tumor-suppressive activity, not only by stabilizing p53 transactivation but also by depressing E1A/E1B-55K-mediated transformation. E1B-55K counteracts this suppressive activity, inducing Sp100A SUMOylation and sequestering the modified cellular factor into the insoluble matrix of the nucleus or into cytoplasmic inclusions. These observations provide novel insights into how E1B-55K modulates cellular determinants to maintain growth-promoting activity during oncogenic processes and lytic infection.

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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Adenovirus Type 5; Region-1b 55-kda Oncoprotein; Cell-transformation; Gene-expression; 55-kilodalton Protein; Sumo Modification; 34-kilodalton Protein; Nuclear-bodies; Messenger-rna; Represses P53

ISSN (print) / ISBN 0950-9232

e-ISSN 0950-9232

Journal Oncogene

Quellenangaben Volume: 35, Issue: 24, Pages: 3178-3189

Publisher Nature Publishing Group

Publishing Place London

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Institute of Virology (VIRO)