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. 2019 May 14;11:1758835919846806. doi: 10.1177/1758835919846806

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© The Author(s), 2019

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 2. — Leptin-induced ICAM-1 expression is mediated through ObR in lung cancer cells.

Leptin-induced increase of ICAM-1 protein (a) and mRNA (c) expression was abolished when ObR was silenced; (b) the silencing effect of siRNA on ObR (siObR) protein expression was confirmed; (d) secreted ICAM-1 enhanced by leptin (100 ng/ml) was reduced by silencing ObR. Graphs show mean ± SD of at least three independent experiments. Control values were used as baseline to normalize the treatment group values.

^**p < 0.01; ^***p < 0.001 compared with the control group.

^#p < 0.05; ^##p < 0.01; ^###p < 0.001 compared with the siCon-transfected leptin-treated group.

Con, control; ICAM-1, intercellular adhesion molecule-1; Lep, leptin; mRNA, messenger ribonucleic acid; SD, ObR, leptin receptor; standard deviation; sICAM-1, soluble ICAM-1; siRNA, small interfering ribonucleic acid; siCon, scrambled control siRNA; siObR, siRNA against ObR.