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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. 6 — Validation of ENO1 and PKM effects on HCC progression and HBV replication in a Murine tumor model. (A) Images of the xenograft tumors in nude mice and the stripped tumor tissues. (B-C) PKM silencing reduced the volume (B) and weight(C) of the xenograft tumors, but was counteracted by ENO1 overexpression. (D-F) By qRT-PCR (D) and Western blot (E, F), PKM silencing suppressed the expression of ENO1, PKM2, PCNA and Ki67 in xenograft tumors, whereas ENO1 overexpression reversed this effect of PKM silencing. (G) Based on immunohistochemistry, the suppression of PKM silencing on the staining of ENO1, PKM2, PCNA and Ki67 proteins in xenograft tumors was abolished by ENO1 overexpression. (H-I) The inhibition of PKM silencing on HBV DNA replication (H) and HBsAg secretion (I) in xenograft tumors was eliminated by ENO1 overexpression. *** P < 0.001 vs. the Control group. ## P < 0.01 vs. the ENO1 group. ^^ P < 0.01 vs. the siPKM group