@article {ANDERSSON2609, author = {BRITTA ANDERSSON and PARVIZ BEHNAM-MOTLAGH and ROGER HENRIKSSON and KJELL GRANKVIST}, title = {Pharmacological Modulation of Lung Cancer Cells for Potassium Ion Depletion}, volume = {25}, number = {4}, pages = {2609--2616}, year = {2005}, publisher = {International Institute of Anticancer Research}, abstract = {Background: Depletion of intracellular potassium ions (K+) is necessary for cells to shrink, induce DNA fragmentation and activate caspases, events which are features of apoptosis. Materials and Methods: We used 86Rb+ as a K+ analogue to evaluate the possibility of pharmacologically depleting human pulmonary mesothelioma (P31) and small cell lung cancer (U1690) cells of K+, for future use in studies of apoptosis induction. Results: The Na+, K+, 2Cl--cotransport inhibitor bumetanide transiently inhibited 86Rb+ influx, but when combined with the Na+, K+, ATPase pump inhibitor ouabain there was a marked and lasting (up to 6 h) 86Rb+ influx inhibition. Cellular K+ efflux was augmented by amphotericin B, digitonin and nigericin. Amphotericin B was an effective 86Rb+ efflux stimulator with low cytotoxicity, whereas digitonin caused cell detachment and nigericin increased LDH release in the U1690 cell line, indicating considerable toxicity of the drugs. Conclusion: It is possible to efficiently reduce intracellular K+ by persistent K+ influx inhibition and simultaneous K+ efflux stimulation with clinically available drugs. Copyright{\textcopyright} 2005 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/25/4/2609}, eprint = {https://ar.iiarjournals.org/content/25/4/2609.full.pdf}, journal = {Anticancer Research} }