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. 2021 Oct 14;14:136. doi: 10.1186/s13048-021-00888-9

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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. 6 — MiR-136 suppressed cell proliferation, migration and invasion, and improved cell sensitivity to PTX and induced cell apoptosis by binding to CBX2 in ovarian cancer. (A and B) The impacts between miR-136 and CBX2 on the IC₅₀ value of PTX were determined by MTT assay in PTX-resistant SKOV3 and HeyA8 cells. (C-E) The effects between miR-136 and CBX2 overexpression on the proliferation of PTX-resistant SKOV3 and HeyA8 cells were determined by CCK-8 and colony formation assays. (F) Flow cytometry analysis was performed to investigate the influences between miR-136 and CBX2 on the apoptosis of PTX-resistant SKOV3 and HeyA8 cells. (G and H) Transwell assay was carried out to investigate the effects between miR-136 and CBX2 on the migration and invasion of PTX-resistant SKOV3 and HeyA8 cells. *P < 0.05