Comparative studies of intracellular Ca2+ in strongly and weakly metastatic rat prostate cancer cell lines

TY - JOUR

T1 - Comparative studies of intracellular Ca2+ in strongly and weakly metastatic rat prostate cancer cell lines

AU - Ding, Y

AU - Robbins, J

AU - Fraser, S P

AU - Grimes, J A

AU - Djamgoz, M B A

PY - 2005/3

Y1 - 2005/3

N2 - The metastatic ability of prostate cancer cells involves differential expression of ionic mechanisms. In the present study, using electrophysiological recordings and intracellular Ca2+ measurements, we investigated Ca2+ related signalling in two rat prostate cancer (MAT-LyLu and AT-2) cell lines of markedly different metastatic potential. Whole-cell voltage clamp experiments indicated the absence of an inward current carried through voltage-dependent Ca2+ channels in either cell line. A Ca2+-dependent component was also absent in the voltage-activated outward K+ currents. Indo-1 microfluorimetry confirmed these results and also revealed marked differences in the resting level of intracellular Ca2+ and the ability of the two cell lines to regulate intracellular Ca2+. The C than the related but strongly metastatic MAT-weakly metastatic AT-2 cells displayed a significantly higher resting intracellular Ca2+ LyLu cell line. Increasing extracellular K+ decreased intracellular Ca2+ in the AT-2 but had no effect on intracellular Ca2+ levels in the MAT-LyLu cells. Furthermore, increasing extracellular Ca2+ increased intracellular Ca2+ in AT-2 but, again, had no effect on MAT-C permeation mechanism operating specifically LyLu cells. These results suggested the presence of a tonic, voltage-independent Ca2+ in the AT-2 cells. The influx of Ca2+ into the AT-2 cells was suppressed by both CdCl2) (100-300 mu M) and SKF-96365 (10-30 mu M). It is concluded that the strongly metastatic MAT-LyLu cell line lacks a voltage-independent basal Ca2+ influx mechanism that is present in the weakly metastatic AT-2 cells. (C) 2005 Elsevier Ltd. All rights reserved

AB - The metastatic ability of prostate cancer cells involves differential expression of ionic mechanisms. In the present study, using electrophysiological recordings and intracellular Ca2+ measurements, we investigated Ca2+ related signalling in two rat prostate cancer (MAT-LyLu and AT-2) cell lines of markedly different metastatic potential. Whole-cell voltage clamp experiments indicated the absence of an inward current carried through voltage-dependent Ca2+ channels in either cell line. A Ca2+-dependent component was also absent in the voltage-activated outward K+ currents. Indo-1 microfluorimetry confirmed these results and also revealed marked differences in the resting level of intracellular Ca2+ and the ability of the two cell lines to regulate intracellular Ca2+. The C than the related but strongly metastatic MAT-weakly metastatic AT-2 cells displayed a significantly higher resting intracellular Ca2+ LyLu cell line. Increasing extracellular K+ decreased intracellular Ca2+ in the AT-2 but had no effect on intracellular Ca2+ levels in the MAT-LyLu cells. Furthermore, increasing extracellular Ca2+ increased intracellular Ca2+ in AT-2 but, again, had no effect on MAT-C permeation mechanism operating specifically LyLu cells. These results suggested the presence of a tonic, voltage-independent Ca2+ in the AT-2 cells. The influx of Ca2+ into the AT-2 cells was suppressed by both CdCl2) (100-300 mu M) and SKF-96365 (10-30 mu M). It is concluded that the strongly metastatic MAT-LyLu cell line lacks a voltage-independent basal Ca2+ influx mechanism that is present in the weakly metastatic AT-2 cells. (C) 2005 Elsevier Ltd. All rights reserved

U2 - 10.1016/j.biocel.2005.07.009

DO - 10.1016/j.biocel.2005.07.009

M3 - Article

VL - 38

SP - 366

EP - 375

JO - International Journal of Biochemistry and Cell Biology

JF - International Journal of Biochemistry and Cell Biology

IS - 3

ER -