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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: ACTN1 promotes HNSCC tumorigenesis and cisplatin resistance by enhancing MYH9-dependent degradation of GSK-3β and integrin β1-mediated phosphorylation of FAK

Fig. 7

β-catenin/c-Myc axis forms a positive feedback loop for enhancing ACTN1 expression in HNSCC. A-B qPCR and western blotting analyses assessing c-Myc and ACTN1 expression in HNSCC cells following siRNA-mediated c-Myc knockdown. C-D qPCR and western blotting analyses of c-Myc and ACTN1 expression in HNSCC cells with c-Myc overexpression. E–F Examination of the effects of c-Myc depletion on the luciferase activities in HNSCC cells transfected with either the wild-type or mutant-type ACTN1 promoter. G-H Assessment of the influence of c-Myc overexpression on luciferase activities in HNSCC cells transfected with either the wild-type or mutant-type ACTN1 promoter. I Enrichment of c-Myc in the ACTN1 promoter region, as revealed by ChIP-qPCR. J Correlation analysis of c-Myc and ACTN1 staining intensities in HNSCC tissues from the in-house cohort. K Western blotting analysis of c-Myc and ACTN1 expression levels in HNSCC cells after β-catenin depletion. L-M Western blotting analysis of c-Myc and ACTN1 expression levels in HNSCC cells treated with the β-catenin signaling activator, BML-284, with or without sic-Myc. ***P < 0.001, ns: not significant

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