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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

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

Fig. 4

ACTN1 mediates activation of β-catenin signaling via the integrin β1-FAK-PI3K-AKT pathway. A Analysis of the interaction between ACTN1 and integrin β1 in SCC-1cisR cells. B-C Influence of ACTN1 depletion or overexpression on phosphorylation and total levels of FAK, PI3K, and AKT. D Western blotting analysis of the effects of integrin β1 depletion on p-FAK, FAK, p-PI3K, PI3K, p-AKT, and AKT expression in ACTN1-overexpressing SCC-1cisR cells. E Assessment of β-catenin and its downstream targets' levels in ACTN1-depleted cells and their controls, treated with or without PF-573228. F Analysis of β-catenin and its downstream targets' expression in control cells and ACTN1-overexpressing cells, with or without PF-573228 administration. G-H Evaluation of the colony-forming potential of HNSCC cells in control and ACTN1-depleted groups, with or without PF-573228 treatment. I-J Assessment of the sphere-forming capacity of HNSCC cells in control and ACTN1-overexpressing groups, with or without PF-573228 treatment. ***P < 0.001, ns: not significant

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