Publication: Targeting the methionine cycle for melanoma therapy with 3-O-(3,4,5-trimethoxybenzoyl)-(-)-epicatechin
Authors
Rodríguez López, José Neptuno ; Sánchez del Campo Ferrer, Luis
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Publisher
WILEY
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DOI
https://doi.org/ 10.1002/ijc.23813
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info:eu-repo/semantics/article
Description
This is an Accepted Manuscript version of the following article, accepted for publication in [International Journal of Cancer]. [Sánchez-del-Campo L, Rodríguez-López JN. Targeting the methionine cycle for melanoma therapy with 3-O-(3,4,5-trimethoxybenzoyl)-(-)-epicatechin. Int J Cancer. 2008 Nov 15;123(10):2446-55. doi: 10.1002/ijc.23813.]. It is deposited under the terms of the Creative Commons Attribution-Non Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
©2008. This manuscript version is made available under the CC-BY-NC 4.0 license http://creativecommons.org/licenses/by-nc/4.0/ This document is the Accepted version of a Published Work that appeared in final form in International Journal of Cancer (IJC). To access the final edited and published work see https://doi.org/ 10.1002/ijc.23813
©2008. This manuscript version is made available under the CC-BY-NC 4.0 license http://creativecommons.org/licenses/by-nc/4.0/ This document is the Accepted version of a Published Work that appeared in final form in International Journal of Cancer (IJC). To access the final edited and published work see https://doi.org/ 10.1002/ijc.23813
Abstract
The higher expression of methionine cycle genes in melanoma cells than in normal melanocytes may be related with increased protein synthesis and transmethylation reactions and the subsequent need for high levels of methionine. 3-O-(3,4,5-trimethoxybenzoyl)-(-)epicatechin (TMECG), a trimethoxy derivative of epicatechin-3-gallate (ECG), effectively suppressed proliferation of melanoma cells in cultures by inducing apoptosis. TMECG modulates the expression of genes involved in methionine metabolism, cellular methylation and glutathione synthesis in.,melanoma cells. TMECG treatment of melanoma cells resulted in the downregulation of antiapoptotic Bcl-2, the upregulation of proapoptotic Bax and the activation of caspase-3; however, it did not induce the expression of the apoptosis protease-activating factor-1 (Apaf-1). Having elucidated the effects of TMECG on the melanoma methionine cycle, we designed therapeuthical strategies to increase its effectiveness. Combinations of TMECG with S-adenosylmethionine or compounds that modulate the intracellular concentration of adenosine strongly increase the anti proliferative effects of TMECG. The ability of TMECG to target multiple aspects related with melanoma survival, with a high degree of potency, points to its clinical value in melanoma therapy.
Citation
International Journal of Cancer (IJC). Volumen123. Inº10. Paginas 2446-2455
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