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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

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

Fig. 2

ACTN1 depletion suppresses malignancy and enhances cisplatin sensitivity of HNSCC cells both in vitro and in vivo. A Assessment of colony formation capacity in HNSCC cells subjected to designated modifications, with or without cisplatin treatment. B Analysis of the tumor sphere-forming ability in HNSCC cells, under specified modifications, and in the presence or absence of cisplatin. C Determination of the apoptosis rate in HNSCC cells following specified modifications, either treated with cisplatin or not. D-F Investigation of tumor size, weight, and volume in xenografts derived from SCC-1cisR cells across different treatment groups. This is coupled with the examination of Ki-67 and CD44 staining intensities within corresponding tumor tissues. G-I Comparative evaluation of tumor size, weight, and volume in xenografts generated by SCC-23cisR cells from specific treatment groups, together with the analysis of Ki-67 and CD44 staining intensities in associated tumor tissues. *P < 0.05, **P < 0.01, ***P < 0.001

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