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. 2017 Jul 17;7:5519. doi: 10.1038/s41598-017-05736-9

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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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Distinct apoptosis mechanisms with cabozantinib removal and with high-dose cabozantinib treatment. (A) Immunoblotting for wild-type CD74-ROS1, F2004V-, or F2075C-mutated cells with or without treatment with 1 μM cabozantinib. Cell lysates were immunoblotted to detect the indicated proteins. (B) Mitochondrial depolarization assay by flow cytometry was performed for wild-type CD74-ROS1 cell (treated with 50 μM rotenone or 1 μM cabozantinib), F2004V- or F2075C-mutated cells (with or without 1 μM cabozantib). Rotenone, a mitochondrial electron transport system inhibitor, was used to treat wild-type CD74-ROS1 cells as a positive control. Each value is shown as mean ± SD of three independent experiments. Statistical significance was calculated by a t test; * indicates p < 0.05 and n.s., p ≥ 0.05. Uncropped blots are presented in Supplementary Fig. S11.