Paradoxical effects of the autophagy inhibitor 3-methyladenine on docetaxel-induced toxicity in PC-3 and LNCaP prostate cancer cells

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• 作者：Rebecca D. Pickard ; Briohny H. Spencer…
• 关键词：Docetaxel ; LNCaP ; PC ; 3 ; 3 ; Methyladenine ; Autophagy ; Prostate cancer
• 刊名：Naunyn-Schmiedeberg's Archives of Pharmacology
• 出版年：2015
• 出版时间：July 2015
• 年：2015
• 卷：388
• 期：7
• 页码：793-799
• 全文大小：533 KB
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• 作者单位：Rebecca D. Pickard (1) (2)
  Briohny H. Spencer (1) (2)
  Amelia J. McFarland (1) (2)
  Nijole Bernaitis (1) (2)
  Andrew K. Davey (1) (2)
  Anthony V. Perkins (1) (3)
  Russ Chess-Williams (4)
  Catherine M. McDermott (4)
  Amanda Forbes (4)
  David Christie (5)
  Shailendra Anoopkumar-Dukie (1) (2)
  
  1. Griffith Health Institute, Griffith University, Gold Coast Campus, Gold Coast, Queensland, 4222, Australia
  2. School of Pharmacy, Griffith University, Gold Coast Campus, Gold Coast, Queensland, 4222, Australia
  3. School of Medical Science, Griffith University, Gold Coast Campus, Gold Coast, Queensland, 4222, Australia
  4. Centre for Urology Research, Bond University, Robina, Queensland, 4226, Australia
  5. Genesis CancerCare, Southport, Queensland, 4215, Australia
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Pharmacology and Toxicology
  Neurosciences
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-1912

文摘

Docetaxel was the first chemotherapeutic agent to increase survival time in patients with androgen-resistant prostate cancer. However, it provides only a modest increase in survival and is associated with significant toxicity. Therefore, there is an urgent need to identify potential adjunct therapies. Given the key role of autophagy in both tumour survival and chemoresistance, the impact of autophagy modulation on docetaxel toxicity was tested in vitro. PC-3 and LNCaP cells were pre-treated with the autophagy inhibitor 3-methyladenine (5?mM) and then exposed to various concentrations (0-00?μM) of docetaxel. Cytoxic effects of docetaxel were measured using resazurin reduction to resorufin, whilst autophagy and apoptosis was measured using monodansylcadaverine, annexin V and caspase-3, respectively. Docetaxel produced significant toxicity in PC-3 cells but was not toxic to LNCaP cells. Pre-treatment with the autophagy inhibitor, 3-methyladenine (5?mM) significantly protected PC-3 cells against docetaxel-induced cytotoxicity, increased autophagosome formation and apoptosis measured using monodansylcadaverine, annexin V and caspase-3 fluorescence, respectively. In contrast, 3-methyladenine was toxic by itself in LNCaP cells and also increased autophagic vesicle formation and apoptosis but did not influence docetaxel toxicity in these cells. These paradoxical effects of 3-methyladenine were largely independent of reactive oxygen species production. We show here that modulation of autophagy may influence docetaxel-induced toxicity in prostate cancer cells and these effects may differ between cell lines.