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. 2024 Jul 5;23:137. doi: 10.1186/s12943-024-02049-0

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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. 2 — MELK contributes to the tumorigenesis, progression and spontaneous lung metastasis of HCC. (A) EdU assay confirming that MELK knockdown suppressed the proliferation of HCC cells. (B) CCK-8 assay showing the inhibition of MELK knockdown in the proliferation of SK-HEP1 and HCC-LM3 cells. (C) Colony formation assay showing the suppression of colony formation by MELK knockdown in HCC cells. (D) Transwell migration assay indicating that MELK knockdown impaired the migration of HCC cells. (E-F) WB assay showing the effect of MELK inhibition on the expression of proliferation- and migration-related factors. (G) Difference in the growth of HCC-LM3 tumors with or without MELK knockdown (n = 5/group). (H-I) Differences in tumor weight (H) and tumor volume (I) in HCC-LM3 tumors with or without MELK knockdown (n = 5/group). (J) IHC staining and TUNEL staining showing the effect of MELK inhibition on tumor proliferation, migration and apoptosis. (K) Construction scheme for the orthotopic implantation model of HCC-LM3 tumors in BALB/c nude mice. (L) General visualization and fluorescence imaging showing the difference in HCC-LM3 tumor growth with or without MELK knockdown. (M) The difference in the fluorescence intensity of HCC-LM3 tumors with or without MELK knockdown (n = 5/group). (N) HE staining reflecting pathological differences in tumor progression upon HCC-LM3 MELK knockdown. (O-P) In vivo bioluminescence imaging showing the inhibition of HCC-LM3 MELK in lung metastasis (n = 5/group). (Q) Macroscopic changes in lung metastasis upon HCC-LM3 MELK knockdown. (R) HE staining showing pathological changes in lung metastasis upon HCC-LM3 MELK knockdown. (S) Changes in intrapulmonary metastasis numbers upon HCC-LM3 MELK inhibition (n = 5/group). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001