Fig. 4
AICAR significantly reduces proliferative and invasive capacities of hybrids overexpressing glycolysis genes and down regulate AMPK. A Growth of E6E7, RST and H1-H6 hybrid cells in absence or presence of AICAR treatment (700 μM for 6 days) evaluated by flow cytometry. For each cell line, data are expressed as growth percentage compared to the growth of the corresponding untreated sample (100%). Statistical analyses were performed using a t-test (nonparametric) Mann-Whitney (**p < 0.01, error bars, SD; n = 6 in triplicates). B Invasion of E6E7, RST and H1-H6 hybrid cells post-vehicle (H2O) or AICAR treatment (700 μM for 24 h of pre-treatment) assessed using Matrigel-coated Boyden chambers. Invasion evaluated at T = 18 h. Data were normalized to the number of cells seeded at T0 determined by flow cytometry. Statistical analyses were done using a t-test (nonparametric) Mann-Whitney (*p < 0.05, **p < 0.01, error bars, SD; n = 5 in quadruplicate in each independent experiment). C Comparison of the AMPK expression genes, i.e. PKRKAA1 and PRKAB1 (Wilcoxon rank sum test, p = 0.009524). P corresponds to E6E7 and RST samples altogether and HYB corresponds to H1 to H4 altogether