Deregulated BCL-2 family proteins impact on repair of DNA double-strand breaks and are targets to overcome radioresistance in lung cancer

Deregulated BCL-2 family proteins impact on repair of DNA double-strand breaks and are targets to... J Cancer Res Clin Oncol (2017) 143:1733–1744 DOI 10.1007/s00432-017-2427-1 ORIGINAL ARTICLE – CANCER RESEARCH Deregulated BCL‑2 family proteins impact on repair of DNA double‑strand breaks and are targets to overcome radioresistance in lung cancer 1 1,4 2 Sarah A. Wieczorek · Frank Breitenbuecher · Aashish Soni · 2 1 3 2,4 Katja Paul‑Konietzko · Sophie Ziegler · Ali Sak · George Iliakis · 1,4 Martin Schuler Received: 8 April 2017 / Accepted: 13 April 2017 / Published online: 21 April 2017 © Springer-Verlag Berlin Heidelberg 2017 Abstract in homologous recombination repair and repair of DNA Purpose DNA damage-induced cell death is a major double-strand breaks by error-prone, alternative end-join- effector mechanism of radiotherapy. Aberrant expres- ing. Notably, genetic or pharmacologic targeting of BCL- sion of anti-apoptotic BCL-2 family proteins is frequently xL or MCL-1 effectively sensitized lung cancer cells to observed in lung cancers. Against this background, we radiotherapy. studied radioresistance mediated by BCL-2 family pro- Conclusions In addition to directly suppressing apoptosis, teins at the mechanistic level and its potential as target for BCL-2 family proteins confer long-term survival benefits to radiochemotherapy. irradiated cancer cells associated with utilization of error- Methods Lung cancer models stably expressing BCL-xL prone http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Cancer Research and Clinical Oncology Springer Journals

Deregulated BCL-2 family proteins impact on repair of DNA double-strand breaks and are targets to overcome radioresistance in lung cancer

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Springer-Verlag Berlin Heidelberg
Subject
Medicine & Public Health; Oncology; Cancer Research; Internal Medicine; Hematology
ISSN
0171-5216
eISSN
1432-1335
D.O.I.
10.1007/s00432-017-2427-1
Publisher site
See Article on Publisher Site

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