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. 2020 Jan 21;10:766. doi: 10.1038/s41598-020-57698-0

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© The Author(s) 2020

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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SENP2 down regulation potentiates bortezomib resistance: (A) Schematic view of SENP2 gene sgRNA sequence designed to target its peptidase_C48 domain. (B) DNA chromatograms obtained from Sanger sequencing of SENP2-sgRNA clones, wherein, 3 types of mutations are inserted in peptidase_C48 domain, which are named as Clone A, B, and C. (C) Western blot analysis to detect SENP2 protein expression in SENP2-sgRNA clones A, B, and C, compared to wild type (WT) cells. Here, GAPDH serves as a loading control. (D) SENP2 wild type (WT) cells and SENP2-sgRNA Clone A, B, C cells were treated with 25 nM bortezomib and cell proliferation at different time points were analysed by using CCK8 kit. (E) SENP2 wild type (WT) cells and SENP2-sgRNA clone-A cells were treated with 0, 5, 10, 15, 25 nM of bortezomib for 48 hours. Then, apoptosis was measured by Annexin-V APC/PI double staining.