AKT1 and MYC induce distinctive metabolic fingerprints in human prostate cancer

Cancer cells may overcome growth factor dependence by deregulating oncogenic and/or tumor-suppressor pathways that affect their metabolism, or by activating metabolic pathways de novo with targeted mutations in critical metabolic enzymes. It is unknown whether human prostate tumors develop a similar...

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Autores principales: Priolo, C., Pyne, S., Rose, J., Regan, E.R., Zadra, G., Photopoulos, C., Cacciatore, S., Schultz, D., Scaglia, Natalia, McDunn, J., De Marzo, A.M., Loda, M.
Formato: Articulo
Lenguaje:Inglés
Publicado: 2014
Materias:
MYC
Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/85055
Aporte de:
id I19-R120-10915-85055
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Ciencias Médicas
Cáncer
Espectrometría de Masas
AKT1
MYC
spellingShingle Ciencias Médicas
Cáncer
Espectrometría de Masas
AKT1
MYC
Priolo, C.
Pyne, S.
Rose, J.
Regan, E.R.
Zadra, G.
Photopoulos, C.
Cacciatore, S.
Schultz, D.
Scaglia, Natalia
McDunn, J.
De Marzo, A.M.
Loda, M.
AKT1 and MYC induce distinctive metabolic fingerprints in human prostate cancer
topic_facet Ciencias Médicas
Cáncer
Espectrometría de Masas
AKT1
MYC
description Cancer cells may overcome growth factor dependence by deregulating oncogenic and/or tumor-suppressor pathways that affect their metabolism, or by activating metabolic pathways de novo with targeted mutations in critical metabolic enzymes. It is unknown whether human prostate tumors develop a similar metabolic response to different oncogenic drivers or a particular oncogenic event results in its own metabolic reprogramming. Akt and Myc are arguably the most prevalent driving oncogenes in prostate cancer. Mass spectrometry-based metabolite profiling was performed on immortalized human prostate epithelial cells transformed by AKT1 or MYC, transgenic mice driven by the same oncogenes under the control of a prostate-specific promoter, and human prostate specimens characterized for the expression and activation of these oncoproteins. Integrative analysis of these metabolomic datasets revealed that AKT1 activation was associated with accumulation of aerobic glycolysis metabolites, whereas MYC overexpression was associated with dysregulated lipid metabolism. Selected metabolites that differentially accumulated in the MYC-high versus AKT1-high tumors, or in normal versus tumor prostate tissue by untargeted metabolomics, were validated using absolute quantitation assays. Importantly, the AKT1/MYC status was independent of Gleason grade and pathologic staging. Our fi ndings show how prostate tumors undergo a metabolic reprogramming that refl ects their molecular phenotypes, with implications for the development of metabolic diagnostics and targeted therapeutics.
format Articulo
Articulo
author Priolo, C.
Pyne, S.
Rose, J.
Regan, E.R.
Zadra, G.
Photopoulos, C.
Cacciatore, S.
Schultz, D.
Scaglia, Natalia
McDunn, J.
De Marzo, A.M.
Loda, M.
author_facet Priolo, C.
Pyne, S.
Rose, J.
Regan, E.R.
Zadra, G.
Photopoulos, C.
Cacciatore, S.
Schultz, D.
Scaglia, Natalia
McDunn, J.
De Marzo, A.M.
Loda, M.
author_sort Priolo, C.
title AKT1 and MYC induce distinctive metabolic fingerprints in human prostate cancer
title_short AKT1 and MYC induce distinctive metabolic fingerprints in human prostate cancer
title_full AKT1 and MYC induce distinctive metabolic fingerprints in human prostate cancer
title_fullStr AKT1 and MYC induce distinctive metabolic fingerprints in human prostate cancer
title_full_unstemmed AKT1 and MYC induce distinctive metabolic fingerprints in human prostate cancer
title_sort akt1 and myc induce distinctive metabolic fingerprints in human prostate cancer
publishDate 2014
url http://sedici.unlp.edu.ar/handle/10915/85055
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