Abstract
The objective of this review is to examine the findings that link obstructive sleep apnea (OSA) with cancer and the role played by the cyclooxygenase (COX) pathway in this association. Epidemiological studies in humans suggest a link between OSA and increased cancer incidence and mortality. Studies carried out in animal models have shown that intermittent hypoxia (IH) induces changes in several signaling pathways involved in the regulation of host immunological surveillance that results in tumor establishment and invasion. IH induces the expression of cyclooxygenase 2 (COX-2) that results in an increased synthesis of prostaglandin E2 (PGE2). PGE2 modulates the function of multiple cells involved in immune responses including T lymphocytes, NK cells, dendritic cells, macrophages, and myeloid-derived suppressor cells. In a mouse model blockage of COX-2/PGE2 abrogated the pro-oncogenic effects of IH. Despite the fact that aspirin inhibits PGE2 production and prevents the development of cancer, none of the epidemiological studies that investigated the association of OSA and cancer included aspirin use in the analysis. Studies are needed to investigate the regulation of the COX-2/PGE2 pathway and PGE2 production in patients with OSA, to better define the role of this axis in the physiopathology of OSA and the potential role of aspirin in preventing the development of cancer.
Highlights
Obstructive sleep apnea (OSA) is characterized by recurrent episodes of upper airway[M1] obstruction occurring during sleep, leading to chronic intermittent hypoxia and sleep fragmentation
The results of this study provide support to the hypothesis that the up-regulation of the cyclooxygenase 2 (COX-2)/prostaglandin E2 (PGE2) pathway induced by hypoxia plays a central role in the association of OSA and cancer
Studies carried in animal models have shown that intermittent hypoxia (IH) induces changes in several signaling pathway and transcription factors involved in the regulation of host immunological surveillance that results in tumor establishment and invasion
Summary
Obstructive sleep apnea (OSA) is characterized by recurrent episodes of upper airway[M1] obstruction occurring during sleep, leading to chronic intermittent hypoxia and sleep fragmentation. Evidence accumulated during the last three decades has demonstrated the association of OSA with hypertension, metabolic dysfunction, cognitive dysfunction, and coronary and cerebrovascular artery disease that results in excess mortality [1]. Recent observations support that the excess in mortality detected in OSA may be the consequence of an increased incidence of malignant tumors in these patients [2,3,4,5,6]. The objective of this review is to analyze the mechanisms that seem to be involved in the predisposition of patients with OSA to develop malignant tumors, as well as the potential role that activation of the cyclooxygenase (COX) pathway can play in this association
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