Augmentation of drug-induced cell death by ER protein BRI3BP.
Biochem Biophys Res Commun
; 362(4): 971-5, 2007 Nov 03.
Article
de En
| MEDLINE
| ID: mdl-17765869
ABSTRACT
To determine the contribution of the endoplasmic reticulum (ER) to cell fate decision, we focused on BRI3-binding protein (BRI3BP) residing in this organelle. BRI3BP, when overexpressed, augmented the apoptosis of human embryonic kidney 293T cells challenged with drugs including the anti-cancer agent etoposide. In contrast, the knockdown of BRI3BP reduced the drug-triggered apoptosis. BRI3BP overexpression enhanced both mitochondrial cytochrome c release and caspase-3 activity in etoposide-treated cells. In response to etoposide, the ER reorganized into irregularly shaped lamellae in mock-transfected cells, whereas in BRI3BP-overexpressing cells, such reorganization was not observed. These observations suggest that BRI3BP is involved in the structural dynamics of the ER and affects mitochondrial viability. Taken together, BRI3BP, widely expressed in animal cell types, seems to possess a pro-apoptotic property and can potentiate drug-induced apoptosis.
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Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Protéines de transport
/
Apoptose
/
Réticulum endoplasmique
/
Étoposide
/
Rein
/
Mitochondries
Limites:
Humans
Langue:
En
Journal:
Biochem Biophys Res Commun
Année:
2007
Type de document:
Article
Pays d'affiliation:
Japon