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. 2022 Jan 6;41:11. doi: 10.1186/s13046-021-02220-1

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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. 7 — The combination treatment of KU-177 and BTZ extends the survival of 5TMM3VT MM mice. A KU-177 greatly extended the survival of 5TMMVT mice. B The combination of KU-177 and BTZ significantly improved the survival time of 5TMMVT mice. C Time course of tumor growth originated from ANBL6 WT/DR cells in NOD-SCID mice treated with KU-177 or untreated. D Mean tumor weight of ANBL6 WT/DR xenografts from KU-177-treated or untreated group at day 37 after injection of MM cells. E Photographic images of xenografts in NOD-SCID mice of each group. F Graphic working model illustrates that AHSA1 is a promising therapeutic target for cellular proliferation and proteasome inhibitor resistance in MM. The data are expressed as mean ± SD.*p<0.05, **p<0.01, ***p<0.001