Abstract
| Lingua originale | English |
|---|---|
| pagine (da-a) | 13-19 |
| Numero di pagine | 7 |
| Rivista | Molecular and Cellular Biochemistry |
| Volume | 287(1-2) |
| Stato di pubblicazione | Published - 2006 |
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All Science Journal Classification (ASJC) codes
- Clinical Biochemistry
- Cell Biology
- Genetics
- Molecular Biology
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Bortezomib induces in HepG2 cells IkappaBalpha degradation mediated by caspase-8. / Calvaruso G; Giuliano M; Portanova P; De Blasio A; Vento R; Tesoriere G.
In: Molecular and Cellular Biochemistry, Vol. 287(1-2), 2006, pag. 13-19.Risultato della ricerca: Article
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TY - JOUR
T1 - Bortezomib induces in HepG2 cells IkappaBalpha degradation mediated by caspase-8.
AU - Calvaruso G; Giuliano M; Portanova P; De Blasio A; Vento R; Tesoriere G
AU - Calvaruso, Giuseppe
AU - Tesoriere, Giovanni
AU - Vento, Renza
AU - Giuliano, Michela
AU - De Blasio, Anna
AU - Portanova, Patrizia
PY - 2006
Y1 - 2006
N2 - The present paper demonstrates that the proteasome inhibitor bortezomib, which behaves as an apoptotic agent in hepatoma HepG2 cells, caused in these cells a decrease in IkappaBalpha level and a consequent increase in NF- kappaB activity. The effect already appeared at 4 h of treatment and preceded the onset of apoptosis which was observed at 24 h. Our results demonstrate that bortezomib-induced IkappaBalpha degradation occurred in conjunction with the activation of caspase-8; moreover, the decrease in IkappaBalpha level was prevented in a dose-dependent manner by the addition of z-IETD, a specific inhibitor of caspase-8. Bortezomib caused the same effects in non-tumor Chang liver cells, which were not susceptible to the apoptotic effect of the drug. Our results also show that other proteases, such as caspase-3 and calpains, exerted only a limited effect on IkappaBalpha degradation. These findings suggest that caspase-8 can be involved in the control of IkappaBalpha level. In addition, the activation of caspase-8 can exert, at least in the first phase of treatment with bortezomib, a protective effect in both HepG2 and Chang liver cells, favouring the activation of the survival factor NF-kappaB.
AB - The present paper demonstrates that the proteasome inhibitor bortezomib, which behaves as an apoptotic agent in hepatoma HepG2 cells, caused in these cells a decrease in IkappaBalpha level and a consequent increase in NF- kappaB activity. The effect already appeared at 4 h of treatment and preceded the onset of apoptosis which was observed at 24 h. Our results demonstrate that bortezomib-induced IkappaBalpha degradation occurred in conjunction with the activation of caspase-8; moreover, the decrease in IkappaBalpha level was prevented in a dose-dependent manner by the addition of z-IETD, a specific inhibitor of caspase-8. Bortezomib caused the same effects in non-tumor Chang liver cells, which were not susceptible to the apoptotic effect of the drug. Our results also show that other proteases, such as caspase-3 and calpains, exerted only a limited effect on IkappaBalpha degradation. These findings suggest that caspase-8 can be involved in the control of IkappaBalpha level. In addition, the activation of caspase-8 can exert, at least in the first phase of treatment with bortezomib, a protective effect in both HepG2 and Chang liver cells, favouring the activation of the survival factor NF-kappaB.
UR - http://hdl.handle.net/10447/20116
M3 - Article
VL - 287(1-2)
SP - 13
EP - 19
JO - Molecular and Cellular Biochemistry
JF - Molecular and Cellular Biochemistry
SN - 0300-8177
ER -