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

Renza Vento, Giuseppe Calvaruso, Michela Giuliano, Giovanni Tesoriere, Ornella Pellerito, Patrizia Portanova

Risultato della ricerca: Articlepeer review

15 Citazioni (Scopus)


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.
Lingua originaleEnglish
pagine (da-a)447-450
Numero di pagine4
RivistaOncology Reports
Stato di pubblicazionePublished - 2007

All Science Journal Classification (ASJC) codes

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  • ???subjectarea.asjc.1300.1306???


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