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Human Molecular Genetics Advance Access published online on June 25, 2008
Human Molecular Genetics, doi:10.1093/hmg/ddn185
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© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

ATP modulates PTEN subcellular localization in multiple cancer cell lines

Glenn P. Lobo1,3, Kristin A. Waite1,3,4, Sarah M. Planchon1,3, Todd Romigh1,3, Janet A. Houghton2,4,6 and Charis Eng1,3,4,5,6,*

1 Genomic Medicine Institute and Cleveland Clinic Foundation, Cleveland, OH 2 Department of Cancer Biology, Cleveland Clinic Foundation, Cleveland, OH 3 Lerner Research Institute, and Cleveland Clinic Foundation, Cleveland, OH 4 Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH 5 Department of Genetics, and Case Western Reserve University School of Medicine, Cleveland, OH, USA 6 CASE Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, OH, USA

* Correspondence Charis Eng, MD, PhD Genomic Medicine Institute Cleveland Clinic Lerner Research Institute 9500 Euclid Ave, NE-50 Cleveland, OH 44195 USA Tel: +1 216 444 3440 Fax: +1 216 636 0566 Email: engc{at}ccf.org

Received March 24, 2008; Revised June 24, 2008; Accepted June 24, 2008

The tumor suppressor gene PTEN plays an important somatic role in both hereditary and sporadic breast carcinogenesis. While the role of PTEN's lipid phosphatase activity, as a negative regulator of the cytoplasmic PI3K/Akt pathway is well known, it is now well established that PTEN exists and functions in the nucleus. Multiple mechanisms of regulating PTEN's subcellular localization have been reported. However none are ubiquitous across multiple cancer cell lines and tissue types. We show here that adenosine triphosphate (ATP) regulates PTEN sub-cellular localization in a variety of different cancer cell lines, including those derived from breast, colon and thyroid carcinomas. Cells deficient in ATP show an increased level of nuclear PTEN protein. This increase in PTEN is reversed when cells are supplemented with ATP, ADP, or AMP. In contrast, the addition of the non-hydrolyzable analogue ATP{gamma}S, did not reverse nuclear PTEN protein levels in all the cell types tested. To our knowledge, this is the first report that describes a regulation of PTEN subcellular localization that is not specific to one cell line or tissue type, but appears to be common across a variety of cell lineages.


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G. P. Lobo, K. A. Waite, S. M. Planchon, T. Romigh, N. T. Nassif, and C. Eng
Germline and somatic cancer-associated mutations in the ATP-binding motifs of PTEN influence its subcellular localization and tumor suppressive function
Hum. Mol. Genet., August 1, 2009; 18(15): 2851 - 2862.
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