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. 2019 Dec 2;9:18101. doi: 10.1038/s41598-019-54843-2

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© The Author(s) 2019

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/.

PMC Copyright notice

Secreted OPN promoted the malignant phenotypes of lung cancer cells mediated by the RON signaling pathway. (a,b) Functions of the OPN-overexpressing A549 cells including invasion and migration, respectively, were dramatically inhibited in the presence of OPN-neutralizing antibody (OPN-Ab) respectively compared to IgG-neutralizing antibody (IgG-Ab) control groups (p < 0.01). OPN-overexpressing A549 cells were treated with media containing 20 μg/ml of OPN-Ab and IgG-Ab, respectively, to block the secreted OPN protein. (c,d) The elevated levels of invasion and migration A549 cells by OPN overexpression were abolished after cells were exposed to 10 μM of the RON inhibitor MK8033 (RONi) for 24 hours compared to the control groups (p < 0.001). (e,f) knockdown of RON by siRNA (kd1 and kd2, respectively) in OPN overexpressing A549 cells significantly reduced the invasion and migration capacities of the cells, respectively. The results represent the mean values ± SD. **p < 0.01, ***p < 0.001.