Cargando…

mTOR is a selective effector of the radiation therapy response in androgen receptor-positive prostate cancer

Ionizing radiation (IR) is used frequently in the management of multiple tumor types, including both organ-confined and locally advanced prostate cancer (PCa). Enhancing tumor radiosensitivity could both reduce the amount of radiation required for definitive treatment and improve clinical outcome. A...

Descripción completa

Detalles Bibliográficos
Autores principales: Schiewer, Matthew J, Den, Robert, Hoang, David T, Augello, Michael A, Lawrence, Yaacov R, Dicker, Adam P, Knudsen, Karen E
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Society for Endocrinology 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253653/
https://www.ncbi.nlm.nih.gov/pubmed/21903859
http://dx.doi.org/10.1530/ERC-11-0072
_version_ 1782220756595245056
author Schiewer, Matthew J
Den, Robert
Hoang, David T
Augello, Michael A
Lawrence, Yaacov R
Dicker, Adam P
Knudsen, Karen E
author_facet Schiewer, Matthew J
Den, Robert
Hoang, David T
Augello, Michael A
Lawrence, Yaacov R
Dicker, Adam P
Knudsen, Karen E
author_sort Schiewer, Matthew J
collection PubMed
description Ionizing radiation (IR) is used frequently in the management of multiple tumor types, including both organ-confined and locally advanced prostate cancer (PCa). Enhancing tumor radiosensitivity could both reduce the amount of radiation required for definitive treatment and improve clinical outcome. Androgen suppression therapy improves clinical outcomes when combined with radiation therapy but is associated with significant acute and chronic toxicities; hence, there is a clear need for alternative means to increase the therapeutic window of radiotherapy. Herein, it is demonstrated that the mammalian target of rapamycin (mTOR) inhibitors rapamycin (sirolimus) and temsirolimus limit both hormone therapy (HT)-sensitive and castration-resistant PCa (CRPC) cell proliferation as single agents and have a profound radiosensitization effect when used in combination with IR. Importantly, the observed radiosensitization was influenced by the treatment schedule, in which adjuvant administration of mTOR inhibitors was most effective in limiting PCa cell population doubling. This schedule-dependent influence on in vitro treatment outcome was determined to be the result of relative effects on the cell cycle kinetics. Finally, adjuvant administration of either mTOR inhibitor tested after IR significantly decreased clonogenic cell survival of both HT-sensitive and CRPC cells compared with IR alone. Taken together, these data demonstrate that inhibition of mTOR confers a radiosensitization phenotype that is dependent on relative cell cycle kinetics and provide a foundation for clinical assessment.
format Online
Article
Text
id pubmed-3253653
institution National Center for Biotechnology Information
language English
publishDate 2012
publisher Society for Endocrinology
record_format MEDLINE/PubMed
spelling pubmed-32536532012-02-01 mTOR is a selective effector of the radiation therapy response in androgen receptor-positive prostate cancer Schiewer, Matthew J Den, Robert Hoang, David T Augello, Michael A Lawrence, Yaacov R Dicker, Adam P Knudsen, Karen E Endocr Relat Cancer Regular Papers Ionizing radiation (IR) is used frequently in the management of multiple tumor types, including both organ-confined and locally advanced prostate cancer (PCa). Enhancing tumor radiosensitivity could both reduce the amount of radiation required for definitive treatment and improve clinical outcome. Androgen suppression therapy improves clinical outcomes when combined with radiation therapy but is associated with significant acute and chronic toxicities; hence, there is a clear need for alternative means to increase the therapeutic window of radiotherapy. Herein, it is demonstrated that the mammalian target of rapamycin (mTOR) inhibitors rapamycin (sirolimus) and temsirolimus limit both hormone therapy (HT)-sensitive and castration-resistant PCa (CRPC) cell proliferation as single agents and have a profound radiosensitization effect when used in combination with IR. Importantly, the observed radiosensitization was influenced by the treatment schedule, in which adjuvant administration of mTOR inhibitors was most effective in limiting PCa cell population doubling. This schedule-dependent influence on in vitro treatment outcome was determined to be the result of relative effects on the cell cycle kinetics. Finally, adjuvant administration of either mTOR inhibitor tested after IR significantly decreased clonogenic cell survival of both HT-sensitive and CRPC cells compared with IR alone. Taken together, these data demonstrate that inhibition of mTOR confers a radiosensitization phenotype that is dependent on relative cell cycle kinetics and provide a foundation for clinical assessment. Society for Endocrinology 2012-02 /pmc/articles/PMC3253653/ /pubmed/21903859 http://dx.doi.org/10.1530/ERC-11-0072 Text en © 2012 Society for Endocrinology http://www.endocrinology.org/journals/reuselicence/ This is an Open Access article distributed under the terms of the Society for Endocrinology's Re-use Licence (http://www.endocrinology.org/journals/reuselicence/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Regular Papers
Schiewer, Matthew J
Den, Robert
Hoang, David T
Augello, Michael A
Lawrence, Yaacov R
Dicker, Adam P
Knudsen, Karen E
mTOR is a selective effector of the radiation therapy response in androgen receptor-positive prostate cancer
title mTOR is a selective effector of the radiation therapy response in androgen receptor-positive prostate cancer
title_full mTOR is a selective effector of the radiation therapy response in androgen receptor-positive prostate cancer
title_fullStr mTOR is a selective effector of the radiation therapy response in androgen receptor-positive prostate cancer
title_full_unstemmed mTOR is a selective effector of the radiation therapy response in androgen receptor-positive prostate cancer
title_short mTOR is a selective effector of the radiation therapy response in androgen receptor-positive prostate cancer
title_sort mtor is a selective effector of the radiation therapy response in androgen receptor-positive prostate cancer
topic Regular Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253653/
https://www.ncbi.nlm.nih.gov/pubmed/21903859
http://dx.doi.org/10.1530/ERC-11-0072
work_keys_str_mv AT schiewermatthewj mtorisaselectiveeffectoroftheradiationtherapyresponseinandrogenreceptorpositiveprostatecancer
AT denrobert mtorisaselectiveeffectoroftheradiationtherapyresponseinandrogenreceptorpositiveprostatecancer
AT hoangdavidt mtorisaselectiveeffectoroftheradiationtherapyresponseinandrogenreceptorpositiveprostatecancer
AT augellomichaela mtorisaselectiveeffectoroftheradiationtherapyresponseinandrogenreceptorpositiveprostatecancer
AT lawrenceyaacovr mtorisaselectiveeffectoroftheradiationtherapyresponseinandrogenreceptorpositiveprostatecancer
AT dickeradamp mtorisaselectiveeffectoroftheradiationtherapyresponseinandrogenreceptorpositiveprostatecancer
AT knudsenkarene mtorisaselectiveeffectoroftheradiationtherapyresponseinandrogenreceptorpositiveprostatecancer