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BioMed Research International
Volume 2015, Article ID 121826, 14 pages
http://dx.doi.org/10.1155/2015/121826
Review Article

Roles of Autophagy Induced by Natural Compounds in Prostate Cancer

V. Naponelli,1,2,3 A. Modernelli,1,2 S. Bettuzzi,1,2,3 and F. Rizzi1,2,3

1Department of Biomedicine, Biotechnology and Translational Research, University of Parma, Via Volturno 39/a, 43125 Parma, Italy
2Centre for Molecular and Translational Oncology (COMT), University of Parma, Parco Area delle Scienze 11/a, 43124 Parma, Italy
3National Institute of Biostructure and Biosystems (INBB), Viale Medaglie d’Oro 305, 00136 Rome, Italy

Received 9 July 2014; Accepted 23 December 2014

Academic Editor: Arkadiusz Orzechowski

Copyright © 2015 V. Naponelli et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Autophagy is a homeostatic mechanism through which intracellular organelles and proteins are degraded and recycled in response to increased metabolic demand or stress. Autophagy dysfunction is often associated with many diseases, including cancer. Because of its role in tumorigenesis, autophagy can represent a new therapeutic target for cancer treatment. Prostate cancer (PCa) is one of the most common cancers in aged men. The evidence on alterations of autophagy related genes and/or protein levels in PCa cells suggests a potential implication of autophagy in PCa onset and progression. The use of natural compounds, characterized by low toxicity to normal tissue associated with specific anticancer effects at physiological levels in vivo, is receiving increasing attention for prevention and/or treatment of PCa. Understanding the mechanism of action of these compounds could be crucial for the development of new therapeutic or chemopreventive options. In this review we focus on the current evidence showing the capacity of natural compounds to exert their action through autophagy modulation in PCa cells.