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Autophagy modulates the effects of bis-anthracycline WP631 on p53-deficient prostate cancer cells

AuthorsMansilla, Sylvia ; Vizcaíno, Carolina ; Rodríguez-Sánchez, María A.; Priebe, Waldemar; Portugal, José
Issue Date16-Feb-2015
PublisherJohn Wiley & Sons
CitationJournal of Cellular and Molecular Medicine 19(4): 786-798 (2015)
Abstract© 2015 The Authors. Treatment of p53-deficient PC-3 human prostate carcinoma cells with nanomolar concentrations of bis-anthracycline WP631 induced changes in gene expression, which resulted in G2/M cell cycle arrest, autophagy and cell death. The presence of 2-deoxy-D-glucose (2-DG), which induces metabolic stress and autophagy, enhanced the antiproliferative effects of WP631. Changes induced by WP631, 2-DG, or co-treatments with both compounds, in the expression of a variety of genes involved in autophagy and apoptosis were quantified by real-time PCR. They were consistent with a raise in autophagy followed by cell death. Some cells dying from G2/M phase showed features of necrosis like early changes in membrane permeability, while others were dying by apoptosis that occurred in presence of little caspase-3 activity. Our results indicate that WP631 is not only an antiproliferative agent acting on gene transcription, but it can also induce autophagy regardless of the presence of other pro-autophagy stimuli. The development of autophagy seemed to improve the cytotoxicity of WP631 in PC-3 cells. Our results indicate that autophagy would enhance the activity of DNA-binding drugs like WP631 that are potent inhibitors of gene transcription.
Publisher version (URL)http://dx.doi.org/10.1111/jcmm.12402
Identifiersdoi: 10.1111/jcmm.12402
issn: 1582-1838
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