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Perturbation of mitochondrial bioenergetics by polycations counteracts resistance to BRAFE600 inhibition in melanoma cells.
Hall, Arnaldur; Maynard, Scott; Wu, Lin-Ping; Merchut-Maya, Joanna Maria; Strauss, Robert; Moghimi, Seyed Moein; Bartek, Jiri.
Afiliación
  • Hall A; Danish Cancer Society Research Center, DK-2100 Copenhagen, Denmark. Electronic address: ahall@cancer.dk.
  • Maynard S; Danish Cancer Society Research Center, DK-2100 Copenhagen, Denmark.
  • Wu LP; Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, People's Republic of China.
  • Merchut-Maya JM; Danish Cancer Society Research Center, DK-2100 Copenhagen, Denmark.
  • Strauss R; Danish Cancer Society Research Center, DK-2100 Copenhagen, Denmark.
  • Moghimi SM; School of Pharmacy, Newcastle University, Newcastle upon Tyne NE1 7RU, United Kingdom; Division of Stratified Medicine, Biomarkers & Therapeutics, Institute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, Framlington Place, Newcastle upon Tyne NE2 4HH, United Kingdom. El
  • Bartek J; Danish Cancer Society Research Center, DK-2100 Copenhagen, Denmark; Department of Medical Biochemistry and Biophysics, Science for Life Laboratory, Karolinska Institute, 171 65 Solna, Sweden. Electronic address: jb@cancer.dk.
J Control Release ; 309: 158-172, 2019 09 10.
Article en En | MEDLINE | ID: mdl-31348978
Acquired resistance to the oncogenic BRAFE600 inhibitor vemurafenib is a major clinical challenge in the treatment of melanoma. Vemurafenib resistance is poorly understood; however, available evidence indicates that reprogrammed mitochondrial metabolism could contribute to the resistance mechanism. Here we show that synthetic polycations, such as polyethylenimines and poly(l-lysine)s, prevent vemurafenib resistance in melanoma cells through induction of mitochondrial bioenergetic crisis. Polycations accumulate to a higher degree in hyperpolarized mitochondria (i.e. mitochondria with greater negative charge) which partly explains greater cellular uptake and mitochondrial accumulation of polycations in melanoma cells compared with epidermal melanocytes. Combined treatment of polycations and vemurafenib diminishes the metabolic flexibility of melanoma cells, making them unable to shift between glycolysis and mitochondrial oxidative phosphorylation according to energy demands. Thus, polycations exert considerable detrimental effects on melanoma cells at concentrations better tolerated by epidermal melanocytes and act synergistically with vemurafenib in effectuating bioenergetic crisis, DNA damage and cell death selectively in melanoma cells. Mechanistic understanding of this synergy could lead to the development of macromolecular and polymer therapeutics with structural attributes that encompass even greater cancer-specific cytotoxicity, and provide strategies for tailor-made combination therapies.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Resistencia a Antineoplásicos / Polielectrolitos / Vemurafenib / Melanoma / Mitocondrias / Antineoplásicos Límite: Humans Idioma: En Revista: J Control Release Asunto de la revista: FARMACOLOGIA Año: 2019 Tipo del documento: Article Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Resistencia a Antineoplásicos / Polielectrolitos / Vemurafenib / Melanoma / Mitocondrias / Antineoplásicos Límite: Humans Idioma: En Revista: J Control Release Asunto de la revista: FARMACOLOGIA Año: 2019 Tipo del documento: Article Pais de publicación: Países Bajos