Fig. 1
From: CAMKKβ supports growth and viability of epithelial ovarian cancer in vitro and in vivo
Loss of CAMKKβ prevents activation of AMPK and ULK1 in EOC spheroids. a Confirmation of CRISPR/Cas9-mediated knockout of CAMKK2 via western blot in OVCAR8 parental, OVCAR8 CAMKK2 KO, HeyA8 parental, and HeyA8 CAMKK2 KO adherent cells (Adh) and spheroids (Sph). # indicates a non-specific band. Vinculin was used as a loading control. b, c Western blot analysis and densitometric quantification of b AMPKT172 and c ULK1S555 phosphorylation in OVCAR8 parental, OVCAR8 CAMKK2 KO, HeyA8 parental, and HeyA8 CAMKK2 KO cells under adherent and spheroid culture conditions.
Quantified western blot data represent mean normalized phospho-protein abundance ± SEM for n = 5 (p-AMPKT172) or n = 4 (p-ULK1S555) independent experiments. Signal for each phospho-target was normalized against the respective total protein signal. Data are expressed relative to the parental adherent sample, for which the mean was set to 1. Data were analyzed via two-way ANOVA and groups with shared lineage (e.g., parental Adh vs. parental Sph) or shared culture condition (e.g., parental Adh vs. CAMKK2 KO Adh) were compared using the Holm-Šídák method (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).
