Bortezomib induces in HepG2 cells IkappaBalpha degradation mediated by caspase-8.

Calvaruso G; Giuliano M; Portanova P; De Blasio A; Vento R; Tesoriere G

Risultato della ricerca: Article

23 Citazioni (Scopus)

Abstract

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.
Lingua originaleEnglish
pagine (da-a)13-19
Numero di pagine7
RivistaMolecular and Cellular Biochemistry
Volume287(1-2)
Stato di pubblicazionePublished - 2006

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Caspase 8
Hep G2 Cells
Degradation
NF-kappa B
Chemical activation
Liver
Proteasome Inhibitors
Calpain
Caspase 3
Peptide Hydrolases
Apoptosis
Hepatocellular Carcinoma
Bortezomib
NF-KappaB Inhibitor alpha
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Clinical Biochemistry
  • Cell Biology
  • Genetics
  • Molecular Biology

Cita questo

Calvaruso G; Giuliano M; Portanova P; De Blasio A; Vento R; Tesoriere G (2006). Bortezomib induces in HepG2 cells IkappaBalpha degradation mediated by caspase-8. Molecular and Cellular Biochemistry, 287(1-2), 13-19.

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

Calvaruso G; Giuliano M; Portanova P; De Blasio A; Vento R; Tesoriere G 2006, 'Bortezomib induces in HepG2 cells IkappaBalpha degradation mediated by caspase-8.', Molecular and Cellular Biochemistry, vol. 287(1-2), pagg. 13-19.
Calvaruso G; Giuliano M; Portanova P; De Blasio A; Vento R; Tesoriere G. Bortezomib induces in HepG2 cells IkappaBalpha degradation mediated by caspase-8. Molecular and Cellular Biochemistry. 2006;287(1-2):13-19.
Calvaruso G; Giuliano M; Portanova P; De Blasio A; Vento R; Tesoriere G. / Bortezomib induces in HepG2 cells IkappaBalpha degradation mediated by caspase-8. In: Molecular and Cellular Biochemistry. 2006 ; Vol. 287(1-2). pagg. 13-19.
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title = "Bortezomib induces in HepG2 cells IkappaBalpha degradation mediated by caspase-8.",
abstract = "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.",
author = "{Calvaruso G; Giuliano M; Portanova P; De Blasio A; Vento R; Tesoriere G} and Giuseppe Calvaruso and Giovanni Tesoriere and Renza Vento and Michela Giuliano and {De Blasio}, Anna and Patrizia Portanova",
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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)

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JO - Molecular and Cellular Biochemistry

JF - Molecular and Cellular Biochemistry

SN - 0300-8177

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