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Fig. 6 | Cancer & Metabolism

Fig. 6

From: Cancer cell metabolic plasticity allows resistance to NAMPT inhibition but invariably induces dependence on LDHA

Fig. 6

The resistant cells are sensitive to l-asparaginase. a CEM PA and CEM RES cells were treated with l-asparaginase (L-Asp) for 48 h. This experiment was performed in normal RPMI-1640 (10% FBS + 2 mM l-glutamine). Percentage of cell viability was determined. b CEM RES cells were treated with 5 nM FK866 and 3 U/ml L-Asp in the presence or absence of Gln supplementation. Twenty-four hours post-treatment, western blot analysis of CHOP expression was conducted. c, d CEM RES cells were treated with 5 nM FK866 and 3 U/ml L-Asp in the presence or absence of Gln supplementation. Twenty-four hours post-treatment, NAD(H) (c) and ATP level (d) were measured. e CEM RES cells were treated with 3 U/ml L-Asp in the presence and absence of Gln supplementation for 24 h. Expression of CHOP, ATF4, and ASNS were determined. Expression of 18S was served as a housekeeping gene. f, g CEM PA and CEM RES cells were treated with 3 U/ml L-Asp in the presence and absence of Gln exposure for 24 h. ATP level (f) and cell viability (g) were measured. Experiments in bg were performed in 20:80 mixture of normal RPMI-1640 (10% FBS + 2 mM l-glutamine) with Eagle’s balanced salt solution (10% FBS). Data were plotted as mean ± S.D. from three independent experiments with technical triplicates (*p < 0.05, **p < 0.01, ***p < 0.001 compared to MOCK) and (ttp < 0.01, tttp < 0.001 compared among treatments)

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