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3. Oxidative stress and antioxidants in the pathophysiology of malignant melanoma

Author

Obrador, Elena, Liu-Smith, Feng, Dellinger, Ryan W, Salvador, Rosario, Meyskens, Frank L, and Estrela, José M

Subjects
Cancer, Prevention, Climate-Related Exposures and Conditions, Animals, Antioxidants, Humans, Melanoma, Oxidation-Reduction, Oxidative Stress, Signal Transduction, intracellular redox state, metastases, reactive nitrogen species, reactive oxygen species, skin cancer, tumor microenvironment, Biochemistry and Cell Biology, Biochemistry & Molecular Biology
Abstract

The high number of somatic mutations in the melanoma genome associated with cumulative ultra violet (UV) exposure has rendered it one of the most difficult of cancers to treat. With new treatment approaches based on targeted and immune therapies, drug resistance has appeared as a consistent problem. Redox biology, including reactive oxygen and nitrogen species (ROS and RNS), plays a central role in all aspects of melanoma pathophysiology, from initiation to progression and to metastatic cells. The involvement of melanin production and UV radiation in ROS/RNS generation has rendered the melanocytic lineage a unique system for studying redox biology. Overall, an elevated oxidative status has been associated with melanoma, thus much effort has been expended to prevent or treat melanoma using antioxidants which are expected to counteract oxidative stress. The consequence of this redox-rebalance seems to be two-fold: on the one hand, cells may behave less aggressively or even undergo apoptosis; on the other hand, cells may survive better after being disseminated into the circulating system or after drug treatment, thus resulting in metastasis promotion or further drug resistance. In this review we summarize the current understanding of redox signaling in melanoma at cellular and systemic levels and discuss the experimental and potential clinic use of antioxidants and new epigenetic redox modifiers.

Published
2019

6. Glioblastoma Therapy: Past, Present and Future

Author

Obrador, Elena, primary, Moreno-Murciano, Paz, additional, Oriol-Caballo, María, additional, López-Blanch, Rafael, additional, Pineda, Begoña, additional, Gutiérrez-Arroyo, Julia Lara, additional, Loras, Alba, additional, Gonzalez-Bonet, Luis G., additional, Martinez-Cadenas, Conrado, additional, Estrela, José M., additional, and Marqués-Torrejón, María Ángeles, additional

Published
2024
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8. Effect of the Mediterranean diet supplemented with nicotinamide riboside and pterostilbene and/or coconut oil on anthropometric variables in amyotrophic lateral sclerosis. A pilot study

Author

Carrera-Juliá, Sandra, primary, Estrela, José M., additional, Zacarés, Mario, additional, Navarro, Mari Ángeles, additional, Vega-Bello, María Jesús, additional, de la Rubia Ortí, José Enrique, additional, Moreno, Mari Luz, additional, and Drehmer, Eraci, additional

Published
2023
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22. Pterostilbene in Cancer Therapy

Author

Obrador, Elena, primary, Salvador-Palmer, Rosario, additional, Jihad-Jebbar, Ali, additional, López-Blanch, Rafael, additional, Dellinger, Thanh H., additional, Dellinger, Ryan W., additional, and Estrela, José M., additional

Published
2021
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24. Nicotinamide Riboside and Pterostilbene Cooperatively Delay Motor Neuron Failure in ALS SOD1G93A Mice

Author

Obrador, Elena, primary, Salvador, Rosario, additional, Marchio, Patricia, additional, López-Blanch, Rafael, additional, Jihad-Jebbar, Ali, additional, Rivera, Pilar, additional, Vallés, Soraya L., additional, Banacloche, Salvador, additional, Alcácer, Javier, additional, Colomer, Nuria, additional, Coronado, Javier A., additional, Alandes, Sandra, additional, Drehmer, Eraci, additional, Benlloch, María, additional, and Estrela, José M., additional

Published
2020
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27. Glutathione and Bcl-2 targeting facilitates elimination by chemoradiotherapy of human A375 melanoma xenografts overexpressing bcl-xl, bcl-2, and mcl-1

Author

Mena Salvador, Rodriguez María L, Ortega Angel, Priego Sonia, Obrador Elena, Asensi Miguel, Petschen Ignacio, Cerdá Miguel, Brown Bob D, and Estrela José M

Subjects
Medicine
Abstract

Abstract Background Bcl-2 is believed to contribute to melanoma chemoresistance. However, expression of Bcl-2 proteins may be different among melanomas. Thus correlations among expression of Bcl-2-related proteins and in vivo melanoma progression, and resistance to combination therapies, was investigated. Methods Human A375 melanoma was injected s.c. into immunodeficient nude mice. Protein expression was studied in tumor samples obtained by laser microdisection. Transfection of siRNA or ectopic overexpression were applied to manipulate proteins which are up- or down-regulated, preferentially, during melanoma progression. Anti-bcl-2 antisense oligonucleotides and chemoradiotherapy (glutathione-depleting agents, paclitaxel protein-binding particles, daunorubicin, X rays) were administered in combination. Results In vivo A375 cells down-regulated pro-apoptotic bax expression; and up-regulated anti-apoptotic bcl-2, bcl-xl, and mcl-1, however only Bcl-2 appeared critical for long-term tumor cell survival and progression in vivo. Reduction of Bcl-2, combined with partial therapies, decreased melanoma growth. But only Bcl-2 targeting plus the full combination of chemoradiotherapy eradicated A375 melanoma, and led to long-term survival (> 120 days) without recurrence in 80% of mice. Tumor regression was not due to immune stimulation. Hematology and clinical chemistry data were within accepted clinical toxicities. Conclusion Strategies to target Bcl-2, may increase the effectiveness of antitumor therapies against melanomas overexpressing Bcl-2 and likely other Bcl-2-related antiapoptotic proteins.

Published
2012
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28. Efficacy and tolerability of EH301 for amyotrophic lateral sclerosis: a randomized, double-blind, placebo-controlled human pilot study

Author

de la Rubia, JosÉ E., primary, Drehmer, Eraci, additional, Platero, JosÉ L., additional, Benlloch, MarÍa, additional, Caplliure-Llopis, Jordi, additional, Villaron-Casales, Carlos, additional, de Bernardo, Nieves, additional, AlarcÓn, Jorge, additional, Fuente, Cristian, additional, Carrera, Sandra, additional, Sancho, David, additional, GarcÍa-Pardo, Pilar, additional, Pascual, Raquel, additional, JuÁrez, Marta, additional, Cuerda-Ballester, María, additional, Forner, Alfonso, additional, Sancho-Castillo, Sandra, additional, Barrios, Carlos, additional, Obrador, Elena, additional, Marchio, Patricia, additional, Salvador, Rosario, additional, Holmes, Holly E., additional, Dellinger, Ryan W., additional, Guarente, Leonard, additional, and Estrela, José M., additional

Published
2019
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34. Role of Natural Stilbenes in the Prevention of Cancer

Author

Sirerol, J. Antoni, Rodríguez, María L., Mena, Salvador, Asensi, Miguel A., Estrela, José M., and Ortega, Angel L.

Subjects
Article Subject
Abstract

Natural stilbenes are an important group of nonflavonoid phytochemicals of polyphenolic structure characterized by the presence of a 1,2-diphenylethylene nucleus. Stilbenes have an extraordinary potential for the prevention and treatment of different diseases, including cancer, due to their antioxidant, cell death activation, and anti-inflammatory properties which associate with low toxicity under in vivo conditions. This review aims to discuss various approaches related to their mechanisms of action, pharmacological activities in animal models and humans, and potential chemoprevention in clinical studies. The biological activity of natural stilbenes is still incompletely understood. Furthermore, after administration to animals or humans, these molecules are rapidly metabolized. Thus pharmacokinetics and/or activities of the natural structures and their metabolites may be very different. Novel drug formulations have been postulated in order to improve stability and bioavailability, to minimize side effects, and to facilitate interaction with their domains in target proteins. These pharmacological improvements should lead stilbenes to become effective candidates as anticancer drugs.

Published
2016
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36. Pterostilbene Decreases the Antioxidant Defenses of Aggressive Cancer Cells In Vivo: A Physiological Glucocorticoids- and Nrf2-Dependent Mechanism

Author

Benlloch, María, primary, Obrador, Elena, additional, Valles, Soraya L., additional, Rodriguez, María L., additional, Sirerol, J. Antoni, additional, Alcácer, Javier, additional, Pellicer, José A., additional, Salvador, Rosario, additional, Cerdá, Concha, additional, Sáez, Guillermo T., additional, and Estrela, José M., additional

Published
2016
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39. Association between Pterostilbene and Quercetin Inhibits Metastatic Activity of B16 Melanoma1

Author

Ferrer, Paula, Asensi, Miguel, Segarra, Ramón, Ortega, Angel, Benlloch, María, Obrador, Elena, Varea, María T, Asensio, Gregorio, Jordá, Leonardo, and Estrela, José M

Subjects
Male, Nitrates, Liver Neoplasms, Melanoma, Experimental, Vascular Cell Adhesion Molecule-1, Hydrogen Peroxide, Integrin alpha4beta1, Mice, Inbred C57BL, Mice, Phenols, Proto-Oncogene Proteins c-bcl-2, Stilbenes, Cell Adhesion, Tumor Cells, Cultured, Animals, Quercetin, Endothelium, Vascular, Nitrites, Research Article
Abstract

Inhibition of cancer growth by resveratrol (trans-3,5,4'-trihydroxystilbene; RESV), a phytoalexin present in many plant species, is limited by its low bioavailability. Pterostilbene (3,5-dimethoxy-4'-hydroxystilbene; PTER) and quercetin (3,3',4',5,6-pentahydroxyflavone; QUER), two structurally related and naturally occurring small polyphenols, show longer half-life in vivo. In vitro growth of highly malignant B16 melanoma F10 cells (B16M-F10) is inhibited (56%) by short-time exposure (60 min/day) to PTER (40 microm) and QUER (20 microm) (approximate mean values of plasma concentrations measured within the first hour after intravenous administration of 20 mg/kg each polyphenol). Intravenous administration of PTER and QUER (20 mg/kg per day) to mice inhibits (73%) metastatic growth of B16M-F10 cell in the liver, a common site for metastasis development. The anti-metastatic mechanism involves: 1) a PTER-induced inhibition of vascular adhesion molecule 1 expression in the hepatic sinusoidal endothelium, which consequently decreases B16M-F10 cell adhesion to the endothelium through very late activation antigen 4; and 2) a QUER- and PTER-induced inhibition of Bcl-2 expression in metastatic cells, which sensitizes them to vascular endothelium-induced cytotoxicity. Our findings demonstrate that the association of PTER and QUER inhibits metastatic melanoma growth and extends host survival.

Published
2005

40. Glucocorticoid Receptor Knockdown Decreases the Antioxidant Protection of B16 Melanoma Cells: An Endocrine System-Related Mechanism that Compromises Metastatic Cell Resistance to Vascular Endothelium-Induced Tumor Cytotoxicity

Author

Obrador, Elena, primary, Valles, Soraya L., additional, Benlloch, María, additional, Sirerol, J. Antoni, additional, Pellicer, José A., additional, Alcácer, Javier, additional, Coronado, Javier Alcácer-F., additional, and Estrela, José M., additional

Published
2014
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41. Pterostilbene-Induced Tumor Cytotoxicity: A Lysosomal Membrane Permeabilization-Dependent Mechanism

Author

Universitat Politècnica de València. Instituto de Reconocimiento Molecular y Desarrollo Tecnológico - Institut de Reconeixement Molecular i Desenvolupament Tecnològic, Mena Llidó, Salvador, Rodriguez, Maria L., Ponsoda Acedo, Javier, Estrela, José M., Jaattela, Marja, ORTEGA, Ángel L., Universitat Politècnica de València. Instituto de Reconocimiento Molecular y Desarrollo Tecnológico - Institut de Reconeixement Molecular i Desenvolupament Tecnològic, Mena Llidó, Salvador, Rodriguez, Maria L., Ponsoda Acedo, Javier, Estrela, José M., Jaattela, Marja, and ORTEGA, Ángel L.

Abstract

The phenolic phytoalexin resveratrol is well known for its health-promoting and anticancer properties. Its potential benefits are, however, limited due to its low bioavailability. Pterostilbene, a natural dimethoxylated analog of resveratrol, presents higher anticancer activity than resveratrol. The mechanisms by which this polyphenol acts against cancer cells are, however, unclear. Here, we show that pterostilbene effectively inhibits cancer cell growth and stimulates apoptosis and autophagosome accumulation in cancer cells of various origins. However, these mechanisms are not determinant in cell demise. Pterostilbene promotes cancer cell death via a mechanism involving lysosomal membrane permeabilization. Different grades of susceptibility were observed among the different cancer cells depending on their lysosomal heat shock protein 70 (HSP70) content, a known stabilizer of lysosomal membranes. A375 melanoma and A549 lung cancer cells with low levels of HSP70 showed high susceptibility to pterostilbene, whereas HT29 colon and MCF7 breast cancer cells with higher levels of HSP70 were more resistant. Inhibition of HSP70 expression increased susceptibility of HT29 colon and MCF7 breast cancer cells to pterostilbene. Our data indicate that lysosomal membrane permeabilization is the main cell death pathway triggered by pterostilbene.

Published
2012

42. Pterostilbene-induced tumor cytotoxicity:a lysosomal membrane permeabilization-dependent mechanism

Author

Mena, Salvador, Rodríguez, María L, Ponsoda, Xavier, Estrela, José M, Jaattela, Marja, Ortega, Angel L, Mena, Salvador, Rodríguez, María L, Ponsoda, Xavier, Estrela, José M, Jaattela, Marja, and Ortega, Angel L

Abstract

The phenolic phytoalexin resveratrol is well known for its health-promoting and anticancer properties. Its potential benefits are, however, limited due to its low bioavailability. Pterostilbene, a natural dimethoxylated analog of resveratrol, presents higher anticancer activity than resveratrol. The mechanisms by which this polyphenol acts against cancer cells are, however, unclear. Here, we show that pterostilbene effectively inhibits cancer cell growth and stimulates apoptosis and autophagosome accumulation in cancer cells of various origins. However, these mechanisms are not determinant in cell demise. Pterostilbene promotes cancer cell death via a mechanism involving lysosomal membrane permeabilization. Different grades of susceptibility were observed among the different cancer cells depending on their lysosomal heat shock protein 70 (HSP70) content, a known stabilizer of lysosomal membranes. A375 melanoma and A549 lung cancer cells with low levels of HSP70 showed high susceptibility to pterostilbene, whereas HT29 colon and MCF7 breast cancer cells with higher levels of HSP70 were more resistant. Inhibition of HSP70 expression increased susceptibility of HT29 colon and MCF7 breast cancer cells to pterostilbene. Our data indicate that lysosomal membrane permeabilization is the main cell death pathway triggered by pterostilbene.

Published
2012

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