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. 2022 Jan 3;41:5. doi: 10.1186/s13046-021-02197-x

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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. 3 — TINCR enhances the resistance to oxaliplatin in HCC cells. A, The survival percentage of HepG2 and HuH7 cells transfected with si-TINCRs or scrambled control, treated with increasing concentration of oxaliplatin (OXA). B-D, Representative images of apoptosis assay of increasing concentration in HepG2 cells transfected with si-TINCRs or scrambled control (B), and quantification in HuH7 (C) and HepG2 (D) cells. E, The survival percentage of HepG2 and HuH7cells transfected with pcDNA3.1-TINCR or empty vector, treated with increasing concentration of OXA. F-H, Representative images apoptosis assays of increasing concentration of OXA in HepG2 cells transfected with pcDNA3.1-TINCR or empty vector (F), and quantification in HuH7 (G) and HepG2 (H) cells. Data are expressed as the mean ± SD of at least three independently repeated experiments. *P < 0.05; **P < 0.01; ***P < 0.001; NS: no significance