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. 2022 May 10;21:111. doi: 10.1186/s12943-022-01549-1

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© The Author(s) 2022

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. 4 — TRAF1 plays a critical role in sunitinib-resistance. A and B Tube formation assay of sunitinib-sensitive cell lines with and without TRAF1 overexpression under sunitinib treatment. C and D Tube formation assay of sunitinib-resistant cell lines with and without TRAF1 knock-down under sunitinib treatment. Representative images (up) and total number of nodes and length (below) are shown. E Correlation analysis of relative RNA expression of TRAF1 with mTOR, VEGFA, p53 and PARP. F Proteins involved in angiogenesis signaling were mediated by TRAF1. G Proteins involved in apoptotic signal pathways were mediated by TRAF1