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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. 8 — MYLK-AS1/miR-424-5p/E2F7 axis positively regulates HCC metastasis, invasion, and angiogenesis via the VEGFR-2 signaling pathway. a E2F7, VEGFR-2, p-VEGFR-2, PLC-λ, p-PLC-λ, Erk1/2, p-Erk1/2, P38, p-P38, FAK, p-FAK, Src, p-Src, Akt, and p-Akt protein expression in Hep-G2 or MHCC-97H cells divided in the following groups: Control, shRNA-NC, shMYLK-AS1-2, NC, and MYLK-AS1. NC represents a blank plasmid control, and MYLK-AS1 is a group overexpressing this lncRNA. The numbers represent the quantification of the relative protein amount. GAPDH was used as the loading control. VEGFR-2 and p-VEGFR-2 protein expression detected after 7-day-co-culture of HUVECs with Hep-G2 or MHCC-97H cells divided in the same groups as above. GAPDH was used as the loading control. b Schematic diagram of the regulatory mechanism of MYLK-AS1/miR-424-5p/E2F7 axis in the promotion of HCC proliferation, metastasis and angiogenesis