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. 2021 Sep 8;40:284. doi: 10.1186/s13046-021-02088-1

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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. 1 — ALKBH5 overexpression promotes EOC cell proliferation and resistance to cisplatin in vitro and in vivo. (a) ALKBH5 mRNA expression is up-regulated in cisplatin-resistant EOC cells (upper); ALKBH5 mRNA expression is up-regulated in platinum-resistan EOC samples (down). (b) Results of the western-blot assays shows ALKBH5 was up-regulated both in cisplatin-resistant EOC cells (upper) and platinum-resistant EOC samples (down). (c) Expression of ALKBH5 protein in platinum-resistant (left) and platinum-sensitive (right) EOC tissues by IHC assay. (d) The transfection efficiency of oe-ALKBH5 lentivirus in A2780 and HO8910. (e and f) CCK8 and EdU proliferation assays confirm that ALKBH5 overexpression promotes cell proliferation in EOC cells. (g) The chemosensitivity assay shows that the IC50 of cisplatin is higher in EOC cells with ALKBH5 overexpression. (h) The IF assay shows that γH2AX expression is reduced in EOC cells with ALKBH5 overexpression after cisplatin treatment (5 μM, 6 h). (i) The cell cycle assays show that ALKBH5 overexpression can attenuate blocking in the G2/M phase induced by cisplatin (5 μM, 48 h). (j) The apoptosis assay shows that ALKBH5 overexpression can decrease the percentage of cell apoptosis induced by cisplatin (5 μM, 48 h). (k) The animal study shows that ALKBH5 overexpression promotes tumor growth and chemoresistance to cisplatin in vivo