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. 2026 Jun 19;24:1144. doi: 10.1186/s12967-026-08468-5

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© The Author(s) 2026

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 4 — Cooperative effects of ENO1 and PKM on HCC cell proliferation, apoptosis, migration, and invasion. (A-C) From CCK-8 (A), EdU incorporation (B) and colony formation (C) assays, PKM silencing suppressed the viability, proliferation and clone formation abilities of HepG2.2.15 cells, which was counteracted by ENO1 overexpression. (D) By TUNEL staining, PKM silencing enhanced the apoptosis of HepG2.2.15 cells, but this influence was abolished by ENO1 overexpression. (E-F) Based on wound healing (E) and Transwell invasion (F) assays, the suppression of PKM silencing on the migration and invasion of HepG2.2.15 cells was reversed by ENO1 overexpression. *** P < 0.001 vs. the Control group. ## P < 0.01 and ### P < 0.001 vs. the ENO1 group. ^^ P < 0.01 vs. the siPKM group