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[Cancer Research 63, 282-286, January 15, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Increased Nuclear Phosphatase and Tensin Homologue Deleted on Chromosome 10 Is Associated with G0-G1 in MCF-7 Cells1

Margaret E. Ginn-Pease and Charis Eng2

Clinical Cancer Genetics Program [C. E.] and Human Cancer Genetics Program [M. E. G-P., C. E.], Comprehensive Cancer Center, Columbus, Ohio 43210; Division of Human Genetics [C. E.], Department of Internal Medicine, Division of Human Cancer Genetics [M. E. G-P., C. E.], Department of Molecular Virology, Immunology and Medical Genetics, and Department of Molecular Genetics [C. E.], The Ohio State University, Columbus, Ohio 43210; and Cancer Research UK Human Cancer Genetics Research Group, University of Cambridge, Cambridge CB2 2XZ, United Kingdom [C. E.]

Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor that causes cell cycle arrest. Lack of a nuclear locator sequence and a function in the cytosolic phosphatidylinositol 3'-kinase/Akt pathway diverted its study from the nucleus. However, immunohistochemistry revealed PTEN in the nucleus of normal cells and decreased nuclear PTEN in neoplastic tissues. Using protein expression analysis and fluoroscopic localization of green fluorescence protein-tagged PTEN, we examined nuclear PTEN in MCF-7 cells. We demonstrate that PTEN enters the nucleus and that nuclear PTEN varies throughout the cell cycle. Higher nuclear PTEN levels were associated with G0-G1 phase, and lower nuclear PTEN levels were associated with S phase. We postulate that nuclear PTEN activity might directly regulate the cell cycle.




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Copyright © 2003 by the American Association for Cancer Research.