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. 2023 Nov 1;55(11):2390–2401. doi: 10.1038/s12276-023-01108-8

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© The Author(s) 2023

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. 6 — a qPCR results showing the expression of cFAM210A and mFAM210A after using cFAM210A-sh lentivirus and its negative control. b CCK-8 assays were performed in cFAM210A-sh HCC cells and their negative controls. c EdU incorporation assays were performed in Huh7 cells (left). Representative images; scale bar, 100 μm (right). d Spheroid formation assays were performed in HepG2 cells (top). Representative images (bottom). e, f In vitro (e) and in vivo (f) limiting dilution assays. The estimated stem cell frequency of each group was calculated by ELDA (http://bioinf.wehi.edu.au/software/elda/); scale bar, 50 μm. g qRT‒PCR showing the expression of seven markers of cancer stem cells in HCC. For (a) and (g), ACTB was used as an endogenous control. For (a–d) and (g), Student’s t test was used. NC negative control, cFAM210A-sh, lentivirus-mediated short hairpin RNA against cFAM210A. ns not significant. *P < 0.05; **P < 0.01; ***P < 0.001.