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. 2020 Nov 9;39:235. doi: 10.1186/s13046-020-01739-z

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© The Author(s) 2020, corrected publication 2023

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. 4 — MYLK-AS1 up-regulates E2F7 expression by competitively binding miR-424-5p in HCC. a-b Binding ability of MYLK-AS1, miR-424-5p, and E2F7 to anti-Ago2 in Hep-G2 and MHCC-97H (anti-igG was used as control) by RIP assay. c HEK-293FT cells co-transfected with wide type (WT) or mutated (Mut) E2F7 3′-UTR reporter vector and miR-424-5p mimic by luciferase reporter assay. d Relative E2F7 mRNA expression in Hep-G2 cells after MYLK-AS1 knockdown or in MHCC-97H cells after MYLK-AS1 overexpression. e E2F7 mRNA expression in MHCC-97H cells after reducing the expression of MYLK-AS1 and/or inhibition of miR-424-5p by qRT-PCR. f E2F7 mRNA expression in MHCC-97H cells following the ectopic expression of miR-424-5p and/or pLVX-E2F7 expression vector lacking the 3′-UTR by qRT-PCR. Results are expressed as mean ± SD. n.s, not significant, *P < 0.05, **P < 0.01, and ***P < 0.001