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. 2023 Aug 16;16:188. doi: 10.1186/s12920-023-01624-6

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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 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. 11 — ATP6V1F influences the migration, invasion, and apoptosis of HCC cells in vitro. A, B Wound healing assay shows that ATP6V1F enhances migration of Hepg2 and SMMC7721 cells. C, D Transwell invasion assay shows that ATP6V1F enhances invasion of Hepg2 and SMMC7721 cells. (E, F) ATP6V1F inhibits apoptosis in Hepg2 and SMMC7721 cells