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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: ATAD3A mediates activation of RAS-independent mitochondrial ERK1/2 signaling, favoring head and neck cancer development

Fig. 3

ATAD3A WA dead mutant functions as a dominant-negative for its oncogenic role in HNSCC cells. A Overexpression of ATAD3A and its WA dead mutant (K358A) in HN12 cells determined by Western blotting. B The effect of overexpression of ATAD3A and its WA dead mutant on cell proliferation on Day 3 in HN12 cells. C The effect of overexpression of ATAD3A and its WA dead mutant on cell colony formation within 3 weeks in HN12 cells. Quantitative data from colony formation assays are shown in the right panel (n = 3). D Overexpression of ATAD3A and its WA dead mutant in ATAD3A KO HN12 cells determined by Western blotting. E The effect of overexpression of ATAD3A and its WA dead mutant on cell proliferation on Day 3 in ATAD3A KO HN12 cells. F The effect of overexpression of ATAD3A and its WA dead mutant on cell colony formation within 3 weeks in ATAD3A KO HN12 cells. Quantitative data from colony formation assays are shown in the right panel (n = 3). G The effects of ATAD3A KO and overexpression of ATAD3A or its WA dead mutant on 3D cell growth on Day 14 in HN12 cells. Quantitative data from alamarBlue staining are shown in the right panel (n = 3). H The effect of ATAD3A WA dead mutant on HN12-derived tongue tumor growth in NSG mice. Representative scanning images of mice tongue with H&E staining and quantitative tumor volume (n = 5 mice/group) are shown in the right and left panels, respectively. WT: wild-type cells; KO: ATAD3A knockout cells; EV: cells overexpressing empty vector; 3A-WT: cells overexpressing wild-type ATAD3A; 3A-K358: cells overexpressing ATAD3A WA dead mutant. *p < 0.05 versus EV or WT; **p < 0.01 versus EV or WT; #p < 0.05 versus KO; ##p < 0.01 versus KO

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