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dc.contributor.authorDing, Y
dc.contributor.authorRobbins, J
dc.contributor.authorFraser, SP
dc.contributor.authorGrimes, JA
dc.contributor.authorDjamgoz, MBA
dc.identifier.citationINTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2006, 38 pp. 366 - 375
dc.description.abstractThe 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.
dc.format.extent366 - 375
dc.titleComparative studies of intracellular Ca2+ in strongly and weakly metastatic rat prostate cancer cell lines
dc.typeJournal Article
rioxxterms.typeJournal Article/Review
pubs.notesaffiliation: Djamgoz, MBA (Reprint Author), Univ London Imperial Coll Sci Technol & Med, Dept Biol Sci, Sir Alexander Fleming Bldg, London SW7 2AZ, England. Univ London Imperial Coll Sci Technol & Med, Dept Biol Sci, London SW7 2AZ, England. Inst Canc Res, Dept Cell & Mol Biol, London SW3 6JB, England. Kings Coll London, Wolfson Ctr Age Related Dis, London SE1 1UL, England. keywords: prostate cancer; AT-2 cells; MAT-LyLu; Ca2+; metastasis keywords-plus: NA+ CHANNEL EXPRESSION; MEDIATED CALCIUM-ENTRY; CARCINOMA-CELLS; CATION CHANNEL; MESSENGER-RNA; IN-VITRO; APOPTOSIS; RECEPTOR; PROLIFERATION; THAPSIGARGIN research-areas: Biochemistry & Molecular Biology; Cell Biology web-of-science-categories: Biochemistry & Molecular Biology; Cell Biology author-email: [email protected] researcherid-numbers: Robbins, Jonathan/A-8661-2008 orcid-numbers: Robbins, Jonathan/0000-0003-1907-0714 funding-acknowledgement: Medical Research Council [G0501019] number-of-cited-references: 57 times-cited: 4 usage-count-last-180-days: 0 usage-count-since-2013: 1 journal-iso: Int. J. Biochem. Cell Biol. doc-delivery-number: 005EP unique-id: ISI:000234805700007 da: 2018-09-04
pubs.notesNot known
pubs.embargo.termsNot known
dc.contributor.icrauthorDing, Yen

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