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. 2020 Sep 11;11(9):741. doi: 10.1038/s41419-020-02967-z

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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. 3 — Total RNA was extracted from the stable HepG2 cells or primary human HCC cells (“HCC1”) with CRISPR/Cas9-LIN28B-AS1-KO construct (“KO-LIN28B-AS1”) or CRISPR/Cas9 control construct (“CRISPR-C”), expression of LIN28B-AS1 a, h, Gli1, Myc and IGF2 mRNA/protein b, i were tested. Cells were further cultured for applied time periods, cell survival, proliferation, migration, invasion as well as cell apoptosis and mitochondrial depolarization were tested by the assays mentioned, and results were quantified c–g, j, k. Listed proteins were quantified and normalized b. Data were presented as mean ± standard deviation (SD, n = 5). *p < 0.05 vs. “CRISPR-C” cells. The experiments were repeated three times, and similar results were obtained.