Figure 3.

The antiproliferative effect of dizocilpine and GYKI52466 can be reproduced by other NMDA and AMPA antagonists in human lung carcinoma (A549) and human rhabdomyosarcoma/medulloblastoma (TE671) cells and is reversed by Ca²⁺ deprivation. A549 (A) and TE671 (C) cells were exposed to either culture medium alone (control), or the NMDA antagonists (+)dizocilpine, (−)dizocilpine, ketamine, or memantine in concentrations ranging from 1 to 500 μM for 96 h, and viability was measured photometrically by means of the MTT assay. Data represent mean normalized optical densities ± SEM of 4–6 trials and were analyzed by means of analysis of variance. The antiproliferative effect of dizocilpine was abolished in Ca²⁺-free medium in lung carcinoma (A) [F_A549(1,37) = 77.10, P < 0.001] and rhabdomyosarcoma/medulloblastoma cells (C) [F_TE671(1,50) = 42.11, P < 0.001]. The antiproliferative effect of (−)dizocilpine was less pronounced in both tumor cell lines compared to the effect of (+)dizocilpine [F_A549(1,80) = 128.52, P < 0.001; F_TE671(1,80) = 268.60, P < 0.001]. (B and D) A549 and TE671 cells were exposed to either culture medium alone (control) or the AMPA antagonists CFM-2 and NBQX in concentrations ranging from 1 to 500 μM for 96 h, and viability was measured photometrically by means of the MTT assay. Data represent mean normalized optical densities ± SEM of 4–6 trials and were analyzed by means of ANOVA. The antiproliferative effect of GYKI52466 was significantly reduced in Ca²⁺-free medium in lung carcinoma (B) [F_A549(1,39) = 51.27, P < 0.001] and abolished in rhabdomyosarcoma/medulloblastoma cells (D) [F_TE671(1,45) = 17.34, P < 0.001].