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. 2022 Jul 7;41(33):3979–3990. doi: 10.1038/s41388-022-02386-8

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© The Author(s) 2022

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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Fig. 2 — A CircME1 was silenced in Caki-1-R cells by two different shRNAs, and the silencing efficiency was determined by qPCR. B CCK8 assay showing that the growth of Caki-1-R cells was suppressed by circME1 knockdown upon sunitinib treatment. C Soft agar colony formation assay showing that circME1 knockdown not only inhibited sunitinib resistance with sunitinib treatment (2 µM), but also repressed proliferation and colony formation without sunitinib treatment. D, E Knockdown of circME1 significantly suppressed the growth and sunitinib resistance of xenograft in vivo. Nude mice with orthotopic tumor were treated with sunitinib (40 mg/kg) or vehicle. The representative bioluminescence images of orthotopic tumors (left panel) and the corresponding statistical analyses (right panel) are shown in D. Other images are shown in Supplementary Fig. S1. The images of gross tumors (upper panel) and the final tumor weights (lower panel) are shown in E. ns not significant, **p < 0.01, ***p < 0.001.