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. 2020 Jul 24;20:338. doi: 10.1186/s12935-020-01419-0

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© The Author(s) 2020

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Establishment of cell line resistant to sunitinib. Tumor size was recorded after nude mice were injected with 786-O, ACHN, first-generation or second-generation tumor cells. The tumor cells in the third-generation were found to resistant to sunitinib (a). The reactions of parental cells (786-O and ACHN) and sunitinib-resistant cells (786-O-R and ACHN-R) to sunitinib were measured by CCK-8 assay. High concentration of sunitinib significantly inhibited the activity of 786-O and ACHN cells (b). Colony formation assay was employed to count the clone number of parental cells and sunitinib-resistant cells after 10 μM of sunitinib or DMSO treatment. Sunitinib at 10 μM markedly repressed the formation of parental cell clones, but had no effect on sunitinib-resistant cells (c). ^*P < 0.05, ^**P < 0.01, compared to NS or 786-O or ACHN group; DMSO, dimethylsulfoxide; NS, normal saline