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Encapsulation of a TRPM8 Agonist, WS12, in Lipid Nanocapsules Potentiates PC3 Prostate Cancer Cell Migration Inhibition through Channel Activation

In prostate carcinogenesis, expression and/or activation of the Transient Receptor Potential Melastatin 8 channel (TRPM8) was shown to block in vitro Prostate Cancer (PCa) cell migration. Because of their localization at the plasma membrane, ion channels, such as TRPM8 and other membrane receptors,...

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Autores principales: Grolez, G. P., Hammadi, M., Barras, A., Gordienko, D., Slomianny, C., Völkel, P., Angrand, P. O., Pinault, M., Guimaraes, C., Potier-Cartereau, M., Prevarskaya, N., Boukherroub, R., Gkika, D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6538610/
https://www.ncbi.nlm.nih.gov/pubmed/31138874
http://dx.doi.org/10.1038/s41598-019-44452-4
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author Grolez, G. P.
Hammadi, M.
Barras, A.
Gordienko, D.
Slomianny, C.
Völkel, P.
Angrand, P. O.
Pinault, M.
Guimaraes, C.
Potier-Cartereau, M.
Prevarskaya, N.
Boukherroub, R.
Gkika, D.
author_facet Grolez, G. P.
Hammadi, M.
Barras, A.
Gordienko, D.
Slomianny, C.
Völkel, P.
Angrand, P. O.
Pinault, M.
Guimaraes, C.
Potier-Cartereau, M.
Prevarskaya, N.
Boukherroub, R.
Gkika, D.
author_sort Grolez, G. P.
collection PubMed
description In prostate carcinogenesis, expression and/or activation of the Transient Receptor Potential Melastatin 8 channel (TRPM8) was shown to block in vitro Prostate Cancer (PCa) cell migration. Because of their localization at the plasma membrane, ion channels, such as TRPM8 and other membrane receptors, are promising pharmacological targets. The aim of this study was thus to use nanocarriers encapsulating a TRPM8 agonist to efficiently activate the channel and therefore arrest PCa cell migration. To achieve this goal, the most efficient TRPM8 agonist, WS12, was encapsulated into Lipid NanoCapsules (LNC). The effect of the nanocarriers on channel activity and cellular physiological processes, such as cell viability and migration, were evaluated in vitro and in vivo. These results provide a proof-of-concept support for using TRPM8 channel-targeting nanotechnologies based on LNC to develop more effective methods inhibiting PCa cell migration in zebrafish xenograft.
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spelling pubmed-65386102019-06-06 Encapsulation of a TRPM8 Agonist, WS12, in Lipid Nanocapsules Potentiates PC3 Prostate Cancer Cell Migration Inhibition through Channel Activation Grolez, G. P. Hammadi, M. Barras, A. Gordienko, D. Slomianny, C. Völkel, P. Angrand, P. O. Pinault, M. Guimaraes, C. Potier-Cartereau, M. Prevarskaya, N. Boukherroub, R. Gkika, D. Sci Rep Article In prostate carcinogenesis, expression and/or activation of the Transient Receptor Potential Melastatin 8 channel (TRPM8) was shown to block in vitro Prostate Cancer (PCa) cell migration. Because of their localization at the plasma membrane, ion channels, such as TRPM8 and other membrane receptors, are promising pharmacological targets. The aim of this study was thus to use nanocarriers encapsulating a TRPM8 agonist to efficiently activate the channel and therefore arrest PCa cell migration. To achieve this goal, the most efficient TRPM8 agonist, WS12, was encapsulated into Lipid NanoCapsules (LNC). The effect of the nanocarriers on channel activity and cellular physiological processes, such as cell viability and migration, were evaluated in vitro and in vivo. These results provide a proof-of-concept support for using TRPM8 channel-targeting nanotechnologies based on LNC to develop more effective methods inhibiting PCa cell migration in zebrafish xenograft. Nature Publishing Group UK 2019-05-28 /pmc/articles/PMC6538610/ /pubmed/31138874 http://dx.doi.org/10.1038/s41598-019-44452-4 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, 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. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Grolez, G. P.
Hammadi, M.
Barras, A.
Gordienko, D.
Slomianny, C.
Völkel, P.
Angrand, P. O.
Pinault, M.
Guimaraes, C.
Potier-Cartereau, M.
Prevarskaya, N.
Boukherroub, R.
Gkika, D.
Encapsulation of a TRPM8 Agonist, WS12, in Lipid Nanocapsules Potentiates PC3 Prostate Cancer Cell Migration Inhibition through Channel Activation
title Encapsulation of a TRPM8 Agonist, WS12, in Lipid Nanocapsules Potentiates PC3 Prostate Cancer Cell Migration Inhibition through Channel Activation
title_full Encapsulation of a TRPM8 Agonist, WS12, in Lipid Nanocapsules Potentiates PC3 Prostate Cancer Cell Migration Inhibition through Channel Activation
title_fullStr Encapsulation of a TRPM8 Agonist, WS12, in Lipid Nanocapsules Potentiates PC3 Prostate Cancer Cell Migration Inhibition through Channel Activation
title_full_unstemmed Encapsulation of a TRPM8 Agonist, WS12, in Lipid Nanocapsules Potentiates PC3 Prostate Cancer Cell Migration Inhibition through Channel Activation
title_short Encapsulation of a TRPM8 Agonist, WS12, in Lipid Nanocapsules Potentiates PC3 Prostate Cancer Cell Migration Inhibition through Channel Activation
title_sort encapsulation of a trpm8 agonist, ws12, in lipid nanocapsules potentiates pc3 prostate cancer cell migration inhibition through channel activation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6538610/
https://www.ncbi.nlm.nih.gov/pubmed/31138874
http://dx.doi.org/10.1038/s41598-019-44452-4
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