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. 2024 Jun 6;22:537. doi: 10.1186/s12967-024-05324-2

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© The Author(s) 2024

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. 6 — HHEX enhances HCC stemness characteristic through SLC17A9. (A) Western blot and qRT-PCR showing expression level of SLC17A9 in SLC17A9-transfected PLC/PRF/5 and Hep3B cells. (B) Summary graphs showed overexpressing SLC17A9 increase the growth rate of shHHEX cells. C.D. Overexpressing SLC17A9 effectively restored the foci formation, migration and invasion in shHHEX cells. E.F. Overexpressing SLC17A9 abrogated the stemness characteristic suppression effects in shHHEX cells