Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 478, Issue 1, Pages 227-233Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.07.063
Keywords
SRC-3; HDAC; Apoptosis; Cancer; AKT; Bcl-2
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Funding
- National Natural Science Foundation of China [81402187, 81371646]
- Ph.D Start-up Fund of Natural Science Foundation of Guangdong Province [2014A030310505]
- Foundation for Distinguished Young Talents in Higher Education of Guangdong [C1085229]
- Fujian Provincial Department of Science Technology [2015J01546]
- Postdoctoral Science Foundation of China [2014M561853]
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SRC-3 is widely expressed in multiple tumor types and involved in cancer cell proliferation and apoptosis. Histone deacetylase (HDAC) inhibitors are promising antitumor drugs. However, the poor efficacy of HDAC inhibitors in solid tumors has restricted its further clinical application. Here, we reported the novel finding that depletion of SRC-3 enhanced sensitivity of breast and lung cancer cells to HDAC inhibitors (SAHA and romidepsin). In contrast, overexpression of SRC-3 decreased SAHA-induced cancer cell apoptosis. Furthermore, we found that SRC-3 inhibitor bufalin increased cancer cell apoptosis induced by HDAC inhibitors. The combination of bufalin and SAHA was particular efficient in attenuating AKT activation and reducing Bcl-2 levels. Taken together, these accumulating data might guide development of new breast and lung cancer therapies. (C) 2016 Elsevier Inc. All rights reserved.
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