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. 2017 Dec 7;5(4):32. doi: 10.3390/medsci5040032

Figure 5.

Figure 5

Figure 5

Single and combination therapies in L3.6pl cells with the spermine synthase inhibitor, CDAP. Altered polyamine pools (expressed as nmoles polyamine/mg protein) and L3.6pl relative % cell growth (vs. an untreated control) were observed after 72 h incubation. Controls were run in parallel, polyamine levels were determined in duplicate, and % cell growth in triplicate. The concentrations of compounds were: DFMO (4.2 mM), CDAP (100 µM in Panels A and C and 1 µM in Panel B), trimer44 PTI (4 µM), and spermidine (Spd, 1 µM). Note: in Panel A, we also tested CDAP (100 µM) + Spd (1 µM), which gave 99% relative cell growth and 0.08 ± 0.20, 13.72 ± 0.85, 0.20 ± 0.09, and 14.00 ±0.97 nmol/mg protein for putrescine, spermidine, spermine, and total polyamines, respectively (not shown). This revealed that exogenous spermidine (1 µM) did not further enhance intracellular spermidine levels in the presence of CDAP (100 µM). This observation is consistent with homeostatic control of polyamine levels. In contrast, in the presence of DFMO (4.2 mM), CDAP (100 µM), and exogenous spermidine (1 µM), significant rescue as evidenced by increased cell growth (from 35% to 86%) was observed, which is consistent with the observed increase in intracellular spermidine pools.