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Gabriele et al. J Cancer Metastasis Treat 2018;4:17                 Journal of Cancer
               DOI: 10.20517/2394-4722.2018.06                           Metastasis and Treatment




               Review                                                                        Open Access


               Prostate cancer cells at a therapeutic gunpoint of
               the autophagy process



               Fabio Gabriele, Carolina Martinelli, Sergio Comincini
               Department of Biology and Biotechnology, University of Pavia, Pavia 27100, Italy.

               Correspondence to: Dr. Sergio Comincini, Department of Biology and Biotechnology, University of Pavia, Pavia 27100, Italy.
               E-mail: sergio.comincini@unipv.it
               How to cite this article: Gabriele F, Martinelli C, Comincini S. Prostate cancer cells at a therapeutic gunpoint of the autophagy
               process. J Cancer Metastasis Treat 2018;4:17. http://dx.doi.org/10.20517/2394-4722.2018.06
               Received: 24 Jan 2018    First Decision: 26 Feb 2018    Revised: 6 Mar 2018    Accepted: 26 Mar 2018    Published: 19 Apr 2018

               Science Editors: Chun Hei Antonio Cheung, Lucio Miele    Copy Editor: Jun-Yao Li    Production Editor: Cai-Hong Wang


               Abstract
               In a normal prostate, the process of controling cell death is essential to maintain tissue homeostasis and its inhibition
               may lead to the development of cancer. Androgen receptor signaling plays pivotal roles in the prostate development
               and homeostasis as well as in the progression of prostate cancer. The main treatment for prostate cancer is a
               combination of androgen deprivation therapy (ADT) using anti-androgens and docetaxil administration. However,
               ADT eventually fails due to a pathological unbalance of cell death processes, in particular apoptosis and autophagy.
               As a result prostate tumors may re-grow and progress into the castration resistant stage. The role of autophagy
               in tumorigenesis is complex and it could be a double-edged sword process, as autophagy defects promote cancer
               progression in association with various dangerous cellular processes, while functional autophagy enables cancer cell
               survival under stress and likely contributes to the resistance of treatment. Autophagy is often impaired in prostate
               cancer, due to either activation of the Akt/mTOR pathway, which normally inhibits autophagy, or through allelic loss of
               Beclin-1 (BECN1), an essential autophagy gene. In particular, elucidating the interplay between autophagy and tumor
               cell metabolism will provide unique opportunities to identify new therapeutic targets and to develop synthetically lethal
               treatment strategies that preferentially target cancer cells, while sparing normal tissues.


               Keywords: Prostate cancer, autophagy, androgen deprivation therapy, mTOR, autophagosome, LC3-II, Beclin-1



               PROSTATE CANCER INCIDENCE AND GENETICS
               Prostate cancer is a tumor that develops in the prostate, a gland in the male reproductive system. Most
               prostate cancers are slow growing but there are cases of aggressive forms. Tumor cells may metastasize
               from the prostate to other parts of the body, particularly the bones and lymph nodes. Prostate cancer may
               cause pain, difficulty in urinating, problems during sexual intercourse, or erectile dysfunction. In particular,

                           © The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


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