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. 2022 Mar 30;7:87. doi: 10.1038/s41392-022-00902-6

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© The Author(s) 2022

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — The EZH2 inhibitor GSK126 or lncRNA ELFN1-AS1 ASO sensitizes HCT116/L-OHP to oxaliplatin. a The IC50 values of oxaliplatin in HCT116/L-OHP cells treated with oxaliplatin (10 μM), GSK126, GSK126 + oxaliplatin (10 μM) and DMSO. b The IC50 values of oxaliplatin in HCT116/L-OHP cells treated with oxaliplatin (10 μM), ASO-ELFN1-AS1, ASO + oxaliplatin (10 μM) and DMSO. c HCT116/L-OHP cells were inoculated into four-week-old male BALB/C nude mice. When the tumors became palpable, they were injected with 0.1% DMSO, oxaliplatin, ASO-ELFN1-AS1, GSK126, ASO-ELFN1-AS1 + oxaliplatin or GSK126 + oxaliplatin. The tumor volume and weight were measured. d IHC of MEIS1, FEN1 and Ki67 in the tumors. e Schematic representation of a model for the major molecular mechanisms (left) and drug intervention hypothesis (right) for the ELFN1-AS1-EZH2-DNMT3a/MEIS1/FEN1 axis in CRC. Data are presented as the mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns, no significance