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. 2020 Jan 16;11(1):34. doi: 10.1038/s41419-019-2188-7

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© The Author(s) 2020

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. 4 — a qRT-PCR detected that miR-26a/b-5p levels in Hep G2 cells with DLGAP1-AS1 knockdown were downregulated by transfecting miR-26a/b-5p inhibitors. b ELISA evaluated the efficiency of IL-6 treatment in Hep G2 cells with DLGAP1-AS1 knockdown. c CCK-8 assay showed that both miR-26a/b-5p inhibitors and IL-6 rescued the inhibitory effect on cell proliferation of DLGAP1-AS1 knockdown. d Wound healing assay showed that both miR-26a/b-5p inhibitors and IL-6 rescued the inhibitory effect on cell migration of DLGAP1-AS1 knockdown. e TUNEL assay showed that both miR-26a/b-5p inhibitors and IL-6 rescued the promotional effect on cell apoptosis of DLGAP1-AS1 knockdown. f, g The influences of miR-26a/b-5p knockdown and IL-6 treatment on EMT-related factors in Hep G2 cells with DLGAP1-AS1 knockdown were respectively analyzed using qRT-PCR and WB. All data are presented as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01.