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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

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

Fig. 6

MYH9 depletion mitigates the tumor promoting effects of ACTN1 overexpression in HNSCC. A Western blotting analyses of ACTN1, MYH9, GSK-3β, β-catenin, cyclin D1, BIRC5, E-cadherin, N-cadherin, and CD44 expression in HNSCC cells following indicated treatments. B-C Assessment of relative TOPFlash and FOPFlash activities in HNSCC cells subjected to the indicated modifications. D-E Evaluation of colony-forming and sphere-forming capacities of HNSCC cells following the indicated treatments. F Analysis of the apoptosis rate in HNSCC cells subjected to the indicated treatments. G Assessment of the invasive capabilities of HNSCC cells following the indicated treatments. H-J Analysis of tumor size, weight, and volume in xenografts generated by SCC-1cisR cells from specified treatment groups, and examination of the staining intensities of Ki-67 and CD44 in corresponding tumor tissues. K-M Evaluation of tumor size, weight, and volume in xenografts formed by SCC-23cisR cells from indicated treatment groups, and examination of the staining intensities of Ki-67 and CD44 in the respective tumor tissues. **P < 0.01, ***P < 0.001, ns: not significant

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