TRAP1 regulation of cancer metabolism: dual role as oncogene or tumor suppressor

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• dc.contributor.author Matassa, Danilo Swann
• dc.contributor.author Agliarulo, Ilenia
• dc.contributor.author Avolio, Rosario
• dc.contributor.author Landriscina, Matteo
• dc.contributor.author Esposito, Franca
• dc.date.accessioned 2019-11-19T07:55:55Z
• dc.date.available 2019-11-19T07:55:55Z
• dc.date.issued 2018
• dc.description.abstract Metabolic reprogramming is an important issue in tumor biology. An unexpected inter- and intra-tumor metabolic heterogeneity has been strictly correlated to tumor outcome. Tumor Necrosis Factor Receptor-Associated Protein 1 (TRAP1) is a molecular chaperone involved in the regulation of energetic metabolism in cancer cells. This protein is highly expressed in several cancers, such as glioblastoma, colon, breast, prostate and lung cancers and is often associated with drug resistance. However, TRAP1 is also downregulated in specific tumors, such as ovarian, bladder and renal cancers, where its lower expression is correlated with the worst prognoses and chemoresistance. TRAP1 is the only mitochondrial member of the Heat Shock Protein 90 (HSP90) family that directly interacts with respiratory complexes, contributing to their stability and activity but it is still unclear if such interactions lead to reduced or increased respiratory capacity. The role of TRAP1 is to enhance or suppress oxidative phosphorylation; the effects of such regulation on tumor development and progression are controversial. These observations encourage the study of the mechanisms responsible for the dualist role of TRAP1 as an oncogene or oncosuppressor in specific tumor types. In this review, TRAP1 puzzling functions were recapitulated with a special focus on the correlation between metabolic reprogramming and tumor outcome. We wanted to investigate whether metabolism-targeting drugs can efficiently interfere with tumor progression and whether they might be combined with chemotherapeutics or molecular-targeted agents to counteract drug resistance and reduce therapeutic failure.
• dc.format.mimetype application/pdf
• dc.identifier.citation Matassa DS, Agliarulo I, Avolio R, Landriscina M, Esposito F. TRAP1 regulation of cancer metabolism: dual role as oncogene or tumor suppressor. Genes (Basel). 2018; 9(4):195. DOI 10.3390/genes9040195
• dc.identifier.doi http://dx.doi.org/10.3390/genes9040195
• dc.identifier.issn 2073-4425
• dc.identifier.uri http://hdl.handle.net/10230/42889
• dc.language.iso eng
• dc.publisher MDPI
• dc.relation.ispartof Genes (Basel). 2018; 9(4):195
• dc.rights © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.rights.uri http://creativecommons.org/licenses/by/4.0/
• dc.subject.keyword TRAP1
• dc.subject.keyword Tumor cell metabolism
• dc.subject.keyword Oxidative phosphorylation
• dc.title TRAP1 regulation of cancer metabolism: dual role as oncogene or tumor suppressor
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/publishedVersion