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. 2022 Sep 20;26(1):82–94. doi: 10.1007/s10120-022-01342-5

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Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Inhibition of NOX1 attenuates IL-17A-induced epithelial cells growth, oxidative stress, and stemness of gastric cancer cells. A Cell cycle analysis of AGS cells treated with rhIL-17A and/or GKT137831. B Changes in percentages of apoptotic cells treated with rhIL-17A and/or GKT137831. C ROS levels in AGS cells treated with rhIL-17A and/or GKT137831. D Sphere formation analysis in AGS-derived spheres treated with rhIL-17A and/or GKT137831. Twelve fields were randomly selected for quantification of spheres per 3 wells of a 6-well plate (original magnification = ×40). Data are presented as mean ± SEM. *P < 0.05, **P < 0.01