dexniguldipine and Glioma

Glioma-initiating cells (GIC) are considered the underlying cause of recurrences of aggressive glioblastomas, replenishing the tumor population and undermining the efficacy of conventional chemotherapy. Here we report the discovery that inhibiting T-type voltage-gated Ca

Topics: Amino Acids; Animals; Biological Transport; Brain Neoplasms; Calcium Channel Blockers; Calcium Channels, T-Type; Cell Death; Cell Line, Tumor; Dihydropyridines; Glioma; Humans; Mice; Mycotoxins; Neoplastic Stem Cells; Potassium Channels, Calcium-Activated; Proteomics; Sodium; Unfolded Protein Response

The effects of nifedipine, niguldipine, nimodipine and nitrendipine on the high K+-induced intracellular Ca2+ ([Ca2+]i) transient in dibutyryl cAMP-differentiated neuroblastoma x glioma hybrid NG 108-15 cells were studied by using the fluorescent Ca2+ indicator fura-2. It was observed that nifedipine at the concentration of 50 microM inhibited the high K+-induced [Ca2+]i transient by about 60%; niguldipine at the concentration of 10 microM caused a reduction of about 65% in the high K+-induced calcium signal and a further increase in the concentration up to 50 microM did not result in a significant further reduction in the high K+-induced calcium signal. However, on the other hand, nimodipine and nitrendipine at 50 microM inhibited almost completely the high K+-induced [Ca2+]i transient. Consequently, it was demonstrated in the present study that nimodipine and nitrendipine inhibit both L- and N-type calcium channels and thus seem to be unique among the dihydropyridines examined in their effects on calcium channels in dibutyryl cAMP-differentiated neuroblastoma x glioma hybrid NG 108-15 cells, whereas nifedipine and niguldipine appear to block mainly L-type calcium channels.

Topics: Animals; Bucladesine; Calcium; Calcium Channel Blockers; Calcium Channels; Cell Differentiation; Dihydropyridines; Evoked Potentials; Glioma; Hybrid Cells; Kinetics; Mice; Neuroblastoma; Nimodipine; Nitrendipine; Potassium; Rats