Fig. 3
ACTN1 enhances tumorigenesis and cisplatin resistance in HNSCC cells via activation of β-catenin signaling. A Enrichment of the EMT pathway in the ACTN1-high group across multiple independent HNSCC cohorts, as indicated by GSEA analysis. B Western blotting analysis of SNAI1, SNAI2, TWIST1, ZEB1, Vimentin, N-cadherin, and E-cadherin expression in ACTN1-depleted cells and control cells. C Western blotting analysis of the effect of ACTN1 overexpression on EMT-associated marker levels in HNSCC cells. D Influence of ACTN1 depletion or overexpression on the levels of β-catenin-mediated signaling pathway components and the expression of key mediators in the Notch, Hedgehog, and TGF-β-Smad pathways. E–F Evaluation of tumor characteristics including size, weight, and volume in SCC-1cisR cells following the indicated treatments. G-H Analysis of tumor size, weight, and volume in xenografts formed by SCC-23cisR cells subjected to the specified treatments. **P < 0.01, ***P < 0.001