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Am J Physiol Cell Physiol 277: C708-C716, 1999;
0363-6143/99 $5.00
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Vol. 277, Issue 4, C708-C716, October 1999

Kinetics of cyclocreatine and Na+ cotransport in human breast cancer cells: mechanism of activity

Nimrod Maril1, Hadassa Degani1, Edna Rushkin1, A. Dean Sherry2, and Mildred Cohn3

1 Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel; 2 Department of Chemistry, University of Texas at Dallas, Richardson, Texas 75083-0688; and 3 Department of Biochemistry and Biophysics, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6089

The growth-inhibitory effect of cyclocreatine (CCr) and the kinetics of CCr and Na+ cotransport were investigated in MCF7 human breast cancer cells and its adriamycin-resistant subline with use of 31P- and 23Na-NMR spectroscopy. The growth-inhibitory effect in the resistant line occurred at a lower CCr concentration and was more pronounced than in the wild-type line. This correlated with an ~10-fold higher affinity of CCr to the transporter in the resistant line. The passive diffusion coefficient of CCr was also higher in the resistant line by three- to fourfold. The transport of CCr was accompanied by a rapid increase in intracellular Na+. This increase was found to depend on the rate of CCr transport and varied differently with CCr concentration in the two cell lines. It is proposed that the cotransport of CCr and Na+ followed by increased Na+ concentration, together with the accumulation of the highly charged phosphocyclocreatine, are responsible for cell swelling and death.

phosphorus-31 nuclear magnetic resonance; sodium-23 nuclear magnetic resonance; cell perfusion


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D. Rivenzon-Segal, E. Rushkin, S. Polak-Charcon, and H. Degani
Glucose transporters and transport kinetics in retinoic acid-differentiated T47D human breast cancer cells
Am J Physiol Endocrinol Metab, September 1, 2000; 279(3): E508 - E519.
[Abstract] [Full Text] [PDF]


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