Utilize este identificador para referenciar este registo: https://hdl.handle.net/1822/62064

TítuloLactate Transporters and pH Regulation: Potential Therapeutic Targets in Glioblastomas
Autor(es)Miranda-Gonçalves, Vera
Reis, R. M.
Baltazar, Fátima
Palavras-chaveAnimals
Brain Neoplasms
Carbonic Anhydrases
Glioblastoma
Glycolysis
Humans
Hydrogen-Ion Concentration
Lactic Acid
Monocarboxylic Acid Transporters
Up-Regulation
Acidic microenvironment
Lactate
pH regulators
Warburg effect
carbonic anhydrases (CAs)
glioblastomas
monocarboxylate transporters (MCTs)
Data2016
EditoraBentham Science Publishers
RevistaCurrent Cancer Drug Targets
CitaçãoMiranda-Gonçalves, V., M Reis, R., & Baltazar, F. (2016). Lactate transporters and ph regulation: potential therapeutic targets in glioblastomas. Current cancer drug targets, 16(5), 388-399
Resumo(s)Despite advances in therapy, glioblastoma (GBM) is still the most prevalent and lethal brain tumor. Thus, it is imperative to identify new and effective therapies that could improve the lifetime of these patients. It is known that tumor cells, such as glioblastomas present metabolic reprogramming, named "Warburg effect", recognized nowadays as a hallmark of cancer. This mechanism is associated with a high dependence of tumor cells on the glycolytic metabolism to sustain energy demands and macromolecule synthesis, leading to production of high amounts of lactic and carbonic acids. These metabolic products induce microenvironment acidification, due to up-regulation of several proteins, such as monocarboxylate transporters (MCTs) and carbonic anhydrases (CAs), to maintain the glycolytic phenotype and the intracellular physiological pH. The dependence on glycolytic metabolism and acidic microenvironment on the acquired resistance to standard therapy has been a research focus in glioblastoma therapy response. In this review, we intend to highlight evidence for the importance of lactate transporters and other pH regulators in GBMs, which are frequently overexpressed in GBMs and associated with tumor aggressiveness. Moreover, we will describe how targeting these proteins could constitute new therapeutic strategies to overcome glioma resistance to therapy.
TipoArtigo
URIhttps://hdl.handle.net/1822/62064
DOI10.2174/1568009616666151222150543
ISSN1568-0096
e-ISSN1873-5576
Versão da editorahttp://www.eurekaselect.com/138023/article
Arbitragem científicayes
AcessoAcesso restrito autor
Aparece nas coleções:ICVS - Artigos em revistas internacionais / Papers in international journals

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