1. Inhibition of SRC-3 enhances sensitivity of human cancer cells to histone deacetylase inhibitors
- Author
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Peipei Nie, Baoyan Wu, Tao Zhang, Yanjun Mi, Zhengzhi Zou, Jie Jiang, Xiaoyong Luo, Guojun Geng, Yanchun Wei, and Wenyi Wang
- Subjects
0301 basic medicine ,Cell Survival ,Biophysics ,Apoptosis ,Biochemistry ,Romidepsin ,Nuclear Receptor Coactivator 3 ,03 medical and health sciences ,0302 clinical medicine ,Cell Line, Tumor ,Depsipeptides ,medicine ,Humans ,Gene Silencing ,Lung cancer ,Molecular Biology ,Protein kinase B ,A549 cell ,Depsipeptide ,Antibiotics, Antineoplastic ,Dose-Response Relationship, Drug ,Chemistry ,Bufalin ,Cancer ,Drug Synergism ,Neoplasms, Experimental ,Cell Biology ,medicine.disease ,Molecular biology ,Histone Deacetylase Inhibitors ,030104 developmental biology ,A549 Cells ,030220 oncology & carcinogenesis ,Cancer research ,Histone deacetylase ,medicine.drug - Abstract
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.
- Published
- 2016
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