Oxygen metabolism in oral cancer: HIF and GLUTs (Review)

Abstract

Oral cancer is a significant cause of morbidity and mortality, and has a poor prognosis. This has encouraged additional studies into factors that may affect the development of this disease. The biological behavior of malignant neoplasms is complex. Studies have investigated the energy metabolism of tumor cells, in an endeavor to elucidate the tumor biology. The identification of molecular signatures and mechanisms, in order to understand tumor progression, may facilitate the identification of novel predictive and prognostic markers. Pathways that influence tumor progression, such as those involving hypoxia-inducible factor (HIF) and glucose transporter (GLUT) proteins, have been the targets of recent studies.

Keywords: cancer; carcinoma; facilitative hypoxia-inducible factor-1α; glucose transport proteins; oral cancer; squamous cells.

Figure 1.

Mechanism of action of hypoxia-induced factor 1 (HIF-1) in normoxic and hypoxic environments. PHD, prolyl hydroxylase domain; PRO 402, proline 402; pVHL, von Hippel-Lindau tumor supressor; E3UB, E3 ubiquitin ligase; HRE, hypoxia response element; CA IX, carbonic anhydrase IX; VEGF, vascular endothelial growth factor; PDGF-β, platelet derived growth factor-β; GLUT 1, glucose transporter 1; CSC, cancer stem cell.