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. 2020 Feb 5;10:1854. doi: 10.1038/s41598-020-58906-7

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Effect of CIH on the protein levels of several hypoxia-related genes in a mouse model of LLC. Protein levels were examined in total protein by western blotting. The representative indicators were measured in the lung homogenate (N:nucleus, C:cytoplasm, other:Total). β-actin was used as a control. ^***p < 0.001, ^**p < 0.01 compared with RA controls. RA: room air; CIH: chronic intermittent hypoxia; LLC: Lewis lung carcinoma; Nrf2: the nuclear factor erythroid 2-related factor 2; Glut-1: glucose transporter 1; CA9: carbonic anhydrase IX; PCNA: proliferating cell nuclear antigen; CDK4: cyclin-dependent kinase 4; HIF1a: hypoxia inducible factor 1α; VEGF: vascular endothelial growth factor; mTOR: mammalian target of rapamycin.