大量研究表明阻塞性睡眠呼吸暂停（OSA）能促进肿瘤的发生、发展，慢性间歇性低氧（CIH）是其中的关键因素。虽然，OSA导致的CIH促癌分子机制尚未明确，但可推测CIH状态下的细胞通讯变化是其中的核心环节。miR-197可调控多个下游靶基因发挥促癌作用。本研究预实验发现OSA患者外泌体miR-197高表达，随着无创正压通气（CPAP）治疗后CIH状态的改善，miR-197表达水平降低。因此，我们推测CIH诱导的外泌体miR-197在OSA促癌机制中具有重要作用。本研究拟通过扩大临床样本验证外泌体miR-197及可能的候选miRNA与CIH之间的相关性；探讨CIH诱导的外泌体miR-197对受体细胞生物学行为的影响；利用动物造模研究CIH诱导外泌体miRNA，特别是miR-197在体内作用的分子机制及寻找可能干预措施，也为制定OSA相关肿瘤防治策略及新型药物研发提供理论依据。

A large number of studies have shown that obstructive sleep apnea (OSA) could promote tumor development and progression, during which chronic intermittent hypoxia (CIH) plays a key role. OSA-induced CIH can promote tumor growth through various ways, and the exact molecular mechanism still needs further exploration. However, it is already inferred that the change of cell communication is the central link in CIH-promoted oncogenesis. MiR-197 could promote cancer by regulating multiple downstream target genes. Our pre-experiments have found that exosomal miR-197 was highly expressed in serum of OSA patients and become decreased after CIH was improved by CPAP treatment. Therefore, we speculate that CIH-induced exosomal miR-197 is essential to the tumor promotion mechanism of OSA. Our study aims to verify the relationship of CIH and exosomal miR-197 or other potential miRNAs through an expanding number of clinical cases. Then, we plan to explore the effects of CIH-induced miR-197 on the biological behaviors of receptor cells. Eventually ,we will construct CIH animal models and induce exosome secretion, especially exsomes carrying miR-197, and try to reveal the molecular mechanism of CIH promoted cancer growth in vivo, in the hope of finding potential counterpart interventions. Our study could help clarify the role of cell communication change in the process of OSA promoted tumor development. Meanwhile, this study provides theoretical basis for the establishment OSA-related tumor prevention strategy and the development of new drugs.