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. 2017 Nov 8;7:15108. doi: 10.1038/s41598-017-15159-1

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© The Author(s) 2017

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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ADAM9-regulated genes with vascular remodeling functions. (A) Ingenuity Pathway Analysis, by comparing gene expression in control versus ADAM9 knockdown cells, showed that the gene network functioned in cell death and survival, cardiovascular disease, and hematological disease. (B) Ratio of differential gene expression in microarray analysis (control shGFP Bm7 cells/ ADAM9 knockdown Bm7 cells). (C–E) Western blot of ADAM9, ANGPT2, and VEGFA in control and ADAM9 knockdown cells from Bm7 lung cancer cells (C), Brmx2 lung cancer cells (D), and A549 lung cancer cells (E). (F) Western blot of ADAM9, VEGFA, and ANGPT2 in Bm7 cells treated with BB94 (a broad spectrum of metalloproteinase inhibitor). (G) Western blot of ADAM9, VEGFA, and ANGPT2 in control and ADAM9 knockout Brmx2 cells transiently transfected with plasmids of empty control (E), ADAM9 wild-type (WT), or ADAM9 mutant (MT) (E348A). EF1α or GAPDH served as the loading control in (C–G). Some cropped blots in (C–G) were displayed and the full-length blots were shown in Supplementary Figure 1.