Hsp72 controls bortezomib-induced HepG2 cell death via interaction with pro-apoptotic factors.

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Abstract

The proteasome inhibitor bortezomib is an efficacious inducer of apoptosis in the hepatoma HepG2 cell line. This study shows that bortezomib increased in these cells the level of the survival factor Hsp72 in a time- and dose-dependent manner. In a first phase of treatment, Hsp72 rapidly increased so that at 24 h of incubation with 50 nM bortezomib its level was approximately five-fold higher than the control. In this phase Hsp72 seemed to play a role in preventing HepG2 cell death, since it interacted with and sequestered the pro-apoptotic factors p53, AIF, Bax and Apaf-1. During a second day of treatment, although the nuclear levels of Hsp72, p53 and AIF increased, the interaction of Hsp72 with these factors diminished. In addition, bortezomib induced the activation of caspases, which stimulated Hsp72 degradation. In conclusion, in the second day of treatment with bortezomib the protective ability of Hsp72 decreased thus favouring the appearance of apoptosis.
Original languageEnglish
Pages (from-to)447-450
Number of pages4
JournalOncology Reports
Volume18(2)
Publication statusPublished - 2007

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Hep G2 Cells
Cell Death
Apoptosis
Proteasome Inhibitors
Caspases
Hepatocellular Carcinoma
Cell Survival
Bortezomib
Cell Line

All Science Journal Classification (ASJC) codes

  • Cancer Research
  • Oncology

Cite this

@article{2a6ca2dd435640a492623fa8acfb4349,
title = "Hsp72 controls bortezomib-induced HepG2 cell death via interaction with pro-apoptotic factors.",
abstract = "The proteasome inhibitor bortezomib is an efficacious inducer of apoptosis in the hepatoma HepG2 cell line. This study shows that bortezomib increased in these cells the level of the survival factor Hsp72 in a time- and dose-dependent manner. In a first phase of treatment, Hsp72 rapidly increased so that at 24 h of incubation with 50 nM bortezomib its level was approximately five-fold higher than the control. In this phase Hsp72 seemed to play a role in preventing HepG2 cell death, since it interacted with and sequestered the pro-apoptotic factors p53, AIF, Bax and Apaf-1. During a second day of treatment, although the nuclear levels of Hsp72, p53 and AIF increased, the interaction of Hsp72 with these factors diminished. In addition, bortezomib induced the activation of caspases, which stimulated Hsp72 degradation. In conclusion, in the second day of treatment with bortezomib the protective ability of Hsp72 decreased thus favouring the appearance of apoptosis.",
author = "Giuseppe Calvaruso and Giovanni Tesoriere and Renza Vento and Michela Giuliano and Patrizia Portanova and Ornella Pellerito",
year = "2007",
language = "English",
volume = "18(2)",
pages = "447--450",
journal = "Oncology Reports",
issn = "1021-335X",
publisher = "Spandidos Publications",

}

TY - JOUR

T1 - Hsp72 controls bortezomib-induced HepG2 cell death via interaction with pro-apoptotic factors.

AU - Calvaruso, Giuseppe

AU - Tesoriere, Giovanni

AU - Vento, Renza

AU - Giuliano, Michela

AU - Portanova, Patrizia

AU - Pellerito, Ornella

PY - 2007

Y1 - 2007

N2 - The proteasome inhibitor bortezomib is an efficacious inducer of apoptosis in the hepatoma HepG2 cell line. This study shows that bortezomib increased in these cells the level of the survival factor Hsp72 in a time- and dose-dependent manner. In a first phase of treatment, Hsp72 rapidly increased so that at 24 h of incubation with 50 nM bortezomib its level was approximately five-fold higher than the control. In this phase Hsp72 seemed to play a role in preventing HepG2 cell death, since it interacted with and sequestered the pro-apoptotic factors p53, AIF, Bax and Apaf-1. During a second day of treatment, although the nuclear levels of Hsp72, p53 and AIF increased, the interaction of Hsp72 with these factors diminished. In addition, bortezomib induced the activation of caspases, which stimulated Hsp72 degradation. In conclusion, in the second day of treatment with bortezomib the protective ability of Hsp72 decreased thus favouring the appearance of apoptosis.

AB - The proteasome inhibitor bortezomib is an efficacious inducer of apoptosis in the hepatoma HepG2 cell line. This study shows that bortezomib increased in these cells the level of the survival factor Hsp72 in a time- and dose-dependent manner. In a first phase of treatment, Hsp72 rapidly increased so that at 24 h of incubation with 50 nM bortezomib its level was approximately five-fold higher than the control. In this phase Hsp72 seemed to play a role in preventing HepG2 cell death, since it interacted with and sequestered the pro-apoptotic factors p53, AIF, Bax and Apaf-1. During a second day of treatment, although the nuclear levels of Hsp72, p53 and AIF increased, the interaction of Hsp72 with these factors diminished. In addition, bortezomib induced the activation of caspases, which stimulated Hsp72 degradation. In conclusion, in the second day of treatment with bortezomib the protective ability of Hsp72 decreased thus favouring the appearance of apoptosis.

UR - http://hdl.handle.net/10447/31260

M3 - Article

VL - 18(2)

SP - 447

EP - 450

JO - Oncology Reports

JF - Oncology Reports

SN - 1021-335X

ER -