This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Neeman, M. Articles by Degani, H. Search for Related Content PubMed PubMed Citation Articles by Neeman, M. Articles by Degani, H.

Metabolic Studies of Estrogen- and Tamoxifen-treated Human Breast Cancer Cells by Nuclear Magnetic Resonance Spectroscopy¹

Isotope Department, The Weizmann Institute of Science, 76100 Rehovot, Israel

The effects of 17ß-estradiol treatment versus tamoxifen on the metabolism of human breast cancer T47D-clone 11 cells were studied by noninvasive ³¹P and ¹³C nuclear magnetic resonance techniques. ³¹P nuclear magnetic resonance spectra revealed differences between estrogen and tamoxifen treated cells. The steady state content of phosphorylcholine and of the nucleoside diphosphates was higher in the tamoxifen treated cells by 33 and 140%, respectively, relative to estrogen treated cells. The intracellular pH of 7.2 and the content of the nucleoside triphosphates, P₁, phosphocreatine, glycerolphosphorylcholine, and glycerolphosphorylethanolamine and uridine diphosphoglucose remained the same in both treatments. Glucose utilization and subsequent lactate, glutamate, alanine, and glycerol 3-phosphate synthesis were monitored on line following administration of specifically labeled [¹³C]glucose. In estrogen treated cells the rate of lactate production via glycolysis was 560 fmol/cell/h and the initial rate of ¹³C labeling of the glutamate pool via the Krebs cycle was 6.8 fmol/cell/h. In the tamoxifen treated cells these rates were 2-fold lower, at 250 and 2.9 fmol/cell/h for lactate and glutamate labeling, respectively. In estrogen treated cells, the calculated content of glutamate (19 fmol/cell), alanine (11 fmol/cell), and glycerol 3-phosphate (8 fmol/cell) was higher than in tamoxifen treated cells, where only glutamate labeling was detected (13 fmol/cell). The observed differences in the in vivo kinetics of glucose metabolism may provide a sensitive measure for detecting the response of human breast cancer cells to estrogen versus tamoxifen treatments.

¹ This work was supported by the Israel Cancer Research Fund, the MINERVA Foundation, Munich, Federal Republic of Germany, and the U.S.-Israel Binational Science Foundation.

Received 6/28/88. Revised 10/12/88. Accepted 10/27/88.

This article has been cited by other articles:

				D. Rivenzon-Segal, R. Margalit, and H. Degani Glycolysis as a metabolic marker in orthotopic breast cancer, monitored by in vivo 13C MRS Am J Physiol Endocrinol Metab, October 1, 2002; 283(4): E623 - E630. [Abstract] [Full Text] [PDF]

				M. Sterin, J. S. Cohen, Y. Mardor, E. Berman, and I. Ringel Levels of Phospholipid Metabolites in Breast Cancer Cells Treated with Antimitotic Drugs: A 31P-Magnetic Resonance Spectroscopy Study Cancer Res., October 1, 2001; 61(20): 7536 - 7543. [Abstract] [Full Text] [PDF]

				F. U. Nielsen, P. Daugaard, L. Bentzen, H. Stodkilde-Jorgensen, J. Overgaard, M. R. Horsman, and R. J. Maxwell Effect of Changing Tumor Oxygenation on Glycolytic Metabolism in a Murine C3H Mammary Carcinoma Assessed by in Vivo Nuclear Magnetic Resonance Spectroscopy Cancer Res., July 1, 2001; 61(13): 5318 - 5325. [Abstract] [Full Text] [PDF]

				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]