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. 2021 Sep 17;14:121. doi: 10.1186/s13048-021-00877-y

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© The Author(s) 2021

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. 5 — UBE2S promotes Olaparib resistance via its enzymatic activity. A2780 and SKOV3 cells transfected with PCMV, PCMV-UBE2S (UBE2S), and PCMV-UBE2S-C95S (C95S) were treated with Olaparib (A2780, 15 μM; SKOV3, 30 μM) for 48 h. A The CCK8 assay was performed to detect cell viability. B The protein levels of PARP, cleaved caspase 3, and β-actin were detected by western blot. C and D Quantification of relative protein levels in (B). E Clonogenic assay was performed to determine the colony formation efficiency of A2780 and SKOV3 cells. F Quantification of the number of clones in (E). (Data are mean ± SEM, *p < 0.05, **p < 0.01, n = 3)