Hypoxia and CoCl protect HepG2 cells against serum deprivation- and t-BHP-induced apoptosis: A possible anti-apoptotic role for HIF-1

J.-P. Piret, C. Lecocq, S. Toffoli, N. Ninane, M. Raes, C. Michiels

Research output: Contribution to journalArticle


Hypoxia inducible factor-1 (HIF-1) is the main transcriptional factor activated by hypoxia. Besides the well-described role assigned to HIF-1 in the adaptation of cells to hypoxia, different recent data describe a possible role for HIF-1 in the modulation of apoptosis. However, this precise role is not yet clearly understood. In this study, chemical and physiological hypoxia, which were shown to induce HIF-1α stabilization and HIF-1 activation, were shown to inhibit apoptosis induced in HepG2 cells by two different pro-apoptotic conditions, serum deprivation- and t-BHP-induced oxidative stress. Indeed, hypoxia reduced DNA fragmentation, caspase activation, and PARP cleavage induced by these two pro-apoptotic conditions. These results are very interesting because it is a clear demonstration that hypoxia and chemical hypoxia have a direct protective effect on apoptotic cell death induced by two different stimuli. This observation is an important data in understanding how tumor growth can occur in challenging environmental conditions.
Original languageEnglish
Pages (from-to)340-349
Number of pages10
JournalExperimental Cell Research
Issue number2
Publication statusPublished - 2004


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