间歇性缺氧通过上调蛋白激酶B/哺乳动物雷帕霉素靶蛋白通路促进S180实体瘤的生长

目的 探讨间歇性缺氧(Intermittent hypoxia,IH)对S180实体瘤生长的影响及其可能机制.方法 2018年3—5月,在新疆医科大学动物房购买的8周龄清洁级昆明鼠为研究对象,将16只接种S180实体瘤的小鼠采用随机数字表法分成2组:常氧组(Room air,RA)和IH组,每组8只,IH暴露两周后处死...

Intermittent hypoxia promotes S180 solid tumor growth by upregulating the Akt/mTOR pathway

Objective To investigate the effects of intermittent hypoxia (IH) on the growth of S180 solid tumor and its possible mechanism.Methods Eight-week-old clean-grade Kunming mice purchased in the Animal Room of Xinjiang Medical University FromMarch to May 2018 were selected as the research objects. Sixteen mice inoculated with S180 solid tumor were randomly assigned into 2groups using a random number table: Room air (RA) group and IH group, 8 mice in each group. The mice were sacrificed after twoweeks of IH exposure, tumor tissues were weighed, and the tumor apoptosis was detected by TUNEL staining, and the expressions ofserine/threonine kinase (Akt), p-Akt, mammalian target of rapamycin (mTOR) and p-mTOR in tumor tissues of RA group and IH group were detected by Western blotting.Results The tumor weights of IH group were significantly heavier than those of RA group (P<0.05).The number of apoptotic bodies in tumor tissues of IH group was (81.18±8.92), which was lower than that in RA group [(129.75 ±20.20), P<0.05). The protein expressions of Akt and mTOR in tumor tissues of IH group were not significantly different from those ofRA group. The protein expression levels of p-Akt and p-mTOR in tumor tissues of IH group increased significantly (P<0.05) compared with RA group.Conclusion IH promotes the growth of S180 solid tumors in mice. The mechanism may be related to the up-regulationof Akt/mTOR pathway and the inhibition of the apoptosis of tumor tissues. This study will provide new ideas for the treatment of tumorscombined with obstructive sleep apnea.