Abstract
The heterodimeric transcription factor HIF-1 (hypoxia-inducible factor 1) represents the key mediator of hypoxia response. HIF-1 controls numerous genes of pivotal importance for cellular metabolism, angiogenesis, cell cycle regulation and inhibition of apoptosis. HIF-1 overexpression and enhanced transcriptional activity are linked to tumour initiation and progression. Malfunction of the HIF-1 signalling network has been associated with breast, ovarian and prostate cancers. Elevated reactive oxygen species (ROS), also observed in such tumours, have been implicated in HIF-1 signalling. Deciphering the role of ROS in cancer onset and their involvement in signalling networks should prove invaluable for the design of novel anticancer therapeutics.
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