The purpose of this study was to evaluate whether obstructive sleep apnea (OSA)-related chronic intermittent hypoxia (CIH) influences lung cancer progression and to elucidate the associated mechanisms in a mouse model of lung cancer. C57/BL6 mice in a CIH group were exposed to intermittent hypoxia for two weeks after tumor induction and compared with control mice (room air). Hypoxia inducible factor 1α (HIF-1α), vascular endothelial growth factor (VEGF) and metastasis-related matrix metalloproteinases (MMP) were measured. The expression levels of several hypoxia-related pathway proteins including HIF-1α, Wnt/ß-catenin, the nuclear factor erythroid 2-related factor 2 (Nrf2) and mammalian target of rapamycin-ERK were measured by western blot. The number (P < 0.01) and volume (P < 0.05) of tumors were increased in the CIH group. The activity of MMP-2 was enhanced after CIH treatment. The level of VEGF was increased significantly in the CIH group (p < 0.05). ß-catenin and Nrf2 were translocated to the nucleus and the levels of downstream effectors of Wnt/ß-catenin signaling increased after IH exposure. CIH enhanced proliferative and migratory properties of tumors in a mouse model of lung cancer. ß-catenin and Nrf2 appeared to be crucial mediators of tumor growth.

译文

:这项研究的目的是评估阻塞性睡眠呼吸暂停(OSA)相关的慢性间歇性缺氧(CIH)是否影响肺癌的进展,并阐明肺癌小鼠模型的相关机制。 CIH组中的C57 / BL6小鼠在诱导肿瘤后暴露于间歇性缺氧2周,并与对照小鼠(室内空气)进行比较。测量缺氧诱导因子1α(HIF-1α),血管内皮生长因子(VEGF)和转移相关基质金属蛋白酶(MMP)。用western blot检测HIF-1α,Wnt /β-catenin,核因子红系2相关因子2(Nrf2)和哺乳动物靶标雷帕霉素-ERK等几种缺氧相关途径蛋白的表达水平。 CIH组的肿瘤数目(P <0.01)和肿瘤体积(P <0.05)增加。 CIH处理后,MMP-2的活性增强。 CIH组的VEGF水平显着升高(p <0.05)。 IH暴露后,β-catenin和Nrf2易位至细胞核,Wnt /β-catenin信号传导的下游效应子水平升高。 CIH增强了肺癌小鼠模型中肿瘤的增殖和迁移特性。 ß-catenin和Nrf2似乎是肿瘤生长的关键介质。

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