Abstract
Combining data on mammalian VDAC with those of Poulsen and colleagues (5), a testable model of interpretation arises: cisplatin first opens type-1 porin at the cell membrane to initiate AVD1. After about 12 h, AVDT starts, showing similarity to regulatory volume increase. Finally, cisplatin reaches VDAC at OMM, thus stimulating caspase-dependent AVD2. Differences between WT EATCs and MDR EATCs under study might just rest on different expression levels of VDAC in their cell membranes; however, differences in the expression levels of plasmalemmal VDAC have been stated for normal or prostate cancer cells, respectively, taken from a single patient (3). Effects observed under the influence of the anion channel blocker NS3728 should also be seen under VDAC blockers. Finally, it might be worthwhile to refer to data on a putative opener of VDAC in cell membranes (10).
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