Myc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer cells
Maranto, C., Perconti, G., Contino, F., Rubino, P., Feo, S., Giallongo, A. (2015). Cellular stress induces cap-independent alpha-enolase/MBP-1 translation. FEBS LETTERS, 589(16), 2110-2116 [10.1016/j.febslet.2015.06.030].
Cellular stress induces cap-independent alpha-enolase/MBP-1 translation
MARANTO, Cristina;PERCONTI, Giovanni;CONTINO, Flavia;FEO, Salvatore;
2015-01-01
Abstract
Myc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer cellsFile | Dimensione | Formato | |
---|---|---|---|
10447_168413.pdf
Solo gestori archvio
Dimensione
1.37 MB
Formato
Adobe PDF
|
1.37 MB | Adobe PDF | Visualizza/Apri Richiedi una copia |
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.