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Dipartimento di Medicina Sperimentale e Clinica (F.A., I.P., D.S.) and Dipartimento di Scienze Farmacobiologiche (D.R.), Università di Catanzaro, "Magna Graecia," 88100 Catanzaro, Italy; Dipartimento di Medicina Sperimentale e Patologia (E.F., A.G.) and Dipartimento di Scienze Cliniche (T.M., A.S., E.T., S.F.), Università "La Sapienza," 00161 Roma, Italy; Tinchi Pisticci Hospital (R.B.), 75020 Matera, Italy; and Department of Clinical Biology (L.L.), Institut Gustave-Roussy, 94805 Villejuif Cedex, France
Address all correspondence and requests for reprints to: Sebastiano Filetti, M.D., Università degli Studi di Roma La Sapienza, Dipartimento di Scienze Cliniche, Clinica Medica 2, Viale del Policlinico, 155, 00161 Roma, Italy. E-mail: sebastiano.filetti{at}uniroma1.it.
Sodium/iodide symporter (NIS) expression has recently been described in human breast cancer, with emphasis on its potential exploitation for the treatment of these tumors with radioiodine. In this study, we analyzed the regulation of NIS expression and function in the MCF-7 human breast cancer cell line. Cell exposure to insulin, IGF-I, IGF-II, or prolactin induced significant increases in 125I uptake and the expression of both NIS mRNA and NIS protein. The latter increases were evident after 6 and 12 h of hormonal stimulation, respectively. In immunocytochemistry studies, NIS was detected mainly in the plasma membrane of MCF-7 cells. A low but significant increase in iodide uptake was produced by treatment with activators of the adenylyl cyclase (cAMP) or protein kinase C pathways. Our study demonstrates that: 1) MCF-7 breast cancer cells are capable of active iodide transport that can be stimulated by insulin, IGF-I, IGF-II, or prolactin; 2) both NIS transcript and protein are expressed in these cells, and this expression is also hormonally stimulated; and 3) MCF-7 iodide transport and NIS expression may be influenced by the activation of cAMP or protein kinase C-dependent signaling. These findings increase our understanding of the molecular mechanisms that regulate NIS expression in breast cancer cells, information that is fundamental for future research aimed at the development of targeted radioiodide treatment for this type of cancer.
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  T. Kogai, E. Ohashi, M. S. Jacobs, S. Sajid-Crockett, M. L. Fisher, Y. Kanamoto, and G. A. Brent Retinoic Acid Stimulation of the Sodium/Iodide Symporter in MCF-7 Breast Cancer Cells Is Meditated by the Insulin Growth Factor-I/Phosphatidylinositol 3-Kinase and p38 Mitogen-Activated Protein Kinase Signaling Pathways J. Clin. Endocrinol. Metab., May 1, 2008; 93(5): 1884 - 1892. [Abstract] [Full Text] [PDF]
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 T Kogai, K Taki, and G A Brent Enhancement of sodium/iodide symporter expression in thyroid and breast cancer. Endocr. Relat. Cancer, September 1, 2006; 13(3): 797 - 826. [Abstract] [Full Text] [PDF]
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 O. Dohan, A. De la Vieja, and N. Carrasco Hydrocortisone and Purinergic Signaling Stimulate Sodium/Iodide Symporter (NIS)-Mediated Iodide Transport in Breast Cancer Cells Mol. Endocrinol., May 1, 2006; 20(5): 1121 - 1137. [Abstract] [Full Text] [PDF]
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 C. Puppin, F. D'Aurizio, A. V. D'Elia, L. Cesaratto, G. Tell, D. Russo, S. Filetti, E. Ferretti, E. Tosi, T. Mattei, et al. Effects of Histone Acetylation on Sodium Iodide Symporter Promoter and Expression of Thyroid-Specific Transcription Factors Endocrinology, September 1, 2005; 146(9): 3967 - 3974. [Abstract] [Full Text] [PDF]
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