Obstructive Sleep Apnea Monocytes Exhibit High Levels of Vascular Endothelial Growth Factor Secretion, Augmenting Tumor Progression

• Main Authors: Carolina Cubillos-Zapata (Author), Enrique Hernández-Jiménez (Author), José Avendaño-Ortiz (Author), Victor Toledano (Author), Anibal Varela-Serrano (Author), Isabel Fernández-Navarro (Author), Raquel Casitas (Author), Carlos Carpio (Author), Luis A. Aguirre (Author), Francisco García-Río (Author), Eduardo López-Collazo (Author)
• Format: Book
• Published: Hindawi Limited, 2018-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 0962-9351; 1466-1861; 10.1155/2018/7373921
• Keywords: Pathology; RB1-214
• Source: Mediators of Inflammation, Vol 2018 (2018)

Obstructive sleep apnea (OSA) is a syndrome characterized by repeated pauses in breathing induced by a partial or complete collapse of the upper airways during sleep. Intermittent hypoxia (IH), a hallmark characteristic of OSA, has been proposed to be a major determinant of cancer development, and patients with OSA are at a higher risk of tumors. Both OSA and healthy monocytes have been found to show enhanced HIF1α expression under IH. Moreover, these cells under IH polarize toward a tumor-promoting phenotype in a HIF1α-dependent manner and influence tumor growth via vascular endothelial growth factor (VEGF). Monocytes from patients with OSA increased the tumor-induced microenvironment and exhibited an impaired cytotoxicity in a 3D tumor in vitro model as a result of the increased HIF1α secretion. Adequate oxygen restoration both in vivo (under continuous positive airway pressure treatment, CPAP) and in vitro leads the monocytes to revert the tumor-promoting phenotype, demonstrating the plasticity of the innate immune system and the oxygen recovery relevance in this context.