Comparative studies of intracellular Ca2+ in strongly and weakly metastatic rat prostate cancer cell lines
Date
2006-03ICR Author
Author
Ding, Y
Robbins, J
Fraser, SP
Grimes, JA
Djamgoz, MBA
Type
Journal Article
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Show full item recordAbstract
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.
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Language
eng
License start date
2006-03
Citation
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2006, 38 pp. 366 - 375
Publisher
PERGAMON-ELSEVIER SCIENCE LTD