Abstract
Hypoxia is characterized by an inadequate supply of oxygen to tissues, and hypoxic regions are commonly found in solid tumors. The cellular response to hypoxic conditions is mediated through the activation of hypoxia-inducible factors (HIFs) that control the expression of a large number of target genes. Recent studies have shown that the receptor for advanced glycation end products (RAGE) participates in hypoxia-dependent cellular adaptation. We review recent evidence on the role of RAGE signaling in tumor biology under hypoxic conditions.
Highlights
In association with transcriptional coactivators such as the coactivator binding protein (CBP) and the p300 protein, C-terminal transactivation domain (C-TAD) controls the transcription of hypoxia-inducible factors (HIFs)-1α and HIF-2α target genes while N-terminal transactivation domain (N-TAD) protects these α subunits against oxygen-dependent degradation [24,28]
receptor for advanced glycation end products (RAGE) belongs to the large immunoglobulin superfamily, and its gene is located in the class III major histocompatibility complex (MHC) region on chromosome
The authors did not interrogate RAGE signaling pathways in their study, it is probable that the effect of S100P on cell migration, tumor growth, and metastasis was partially mediated by RAGE
Summary
Hypoxia is a condition characterized by low levels of oxygen in tissues and organs. Two main types of hypoxia have been described: physiological and pathological hypoxia [1]. Physiological hypoxia is observed when oxygen levels are slightly lower than typical under healthy conditions and when these levels can be reversed by homeostatic mechanisms [2]. Pathological hypoxia is characterized by oxygen levels significantly lower than those in healthy tissues and can reach levels of less than 1% oxygen saturation [1]. Pathological hypoxia develops because homeostatic mechanisms are not able to restore the supply of the tissue with oxygen to its physiological level [3]. Pathological hypoxia is observed in many solid tumors and has been shown to contribute to tumor growth, metastasis, and chemoresistance [1,4]. HIFs regulate the transcription of hundreds of genes, some of them critically involved in cancer processes contributing to tumorigenesis, chemoresistance, and metastasis [5,6]
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