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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 6. — Leptin-induced phosphorylation of the signaling cascade is mediated by the JAK1/2/STAT3/FAK/ERK/GSK3αβ axis in lung cancer cells.

By inhibiting JAK1/2 by JAKi, JAK2 by AG490, and STAT3 by Stattic, leptin-induced phosphorylation of FAK (a), ERK (b), and GSK3αβ (c) were all reversed. By inhibiting FAK by PF573228, leptin-induced phosphorylation of ERK (d) and GSK3αβ (e) were both decreased. (f) By inhibiting ERK by U0126, leptin-induced GSK3αβ phosphorylation was decreased. 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 leptin-treated group.

Con, control; AG, AG490; ERK, extracellular signal-regulated kinase; FAK, focal-adhesion kinase; GSK, glycogen synthase kinase; JAK, Janus kinase; JAKi, JAK inhibitor I; p-, phospho; PF, PF573228; SB, SB216763; SD, standard deviation.