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Human Molecular Genetics, 2001, Vol. 10, No. 3 251-258
© 2001 Oxford University Press

Transient ectopic expression of PTEN in thyroid cancer cell lines induces cell cycle arrest and cell type-dependent cell death

Liang-Ping Weng1,2,4, Oliver Gimm1,2,4, Jennifer B. Kum1,2,5, Wendy M. Smith1,2,4, Xiao-Ping Zhou1,2,4, David Wynford-Thomas6, Gustavo Leone2,4 and Charis Eng1,2,3,4,7,+

1Clinical Cancer Genetics and 2Human Cancer Genetics Programs, Comprehensive Cancer Center, 3Division of Human Genetics, Department of Internal Medicine and 4Division of Human Cancer Genetics, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, OH 43210, USA, 5Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA, 6Department of Pathology, University of Wales School of Medicine, Cardiff CF4 4XN, UK and 7Cancer Research Campaign Human Cancer Genetics Research Group, University of Cambridge, Cambridge CB2 2QQ, UK

The tumour suppressor gene PTEN/MMAC1/TEP1 has been implicated in a variety of human cancers and several inherited hamartoma tumour syndromes, including Cowden syndrome, which has a high risk of breast and thyroid cancer. We have previously reported that overexpression of PTEN in MCF-7 breast cancer cells induces cell cycle arrest and apoptosis. In this study, we analysed PTEN status at both the structural and expression levels and explored PTEN’s growth-suppressive effects on thyroid. We found that 1 of 10 thyroid cancer lines [follicular thyroid carcinoma FTC-133] had hemizygous deletion and a splice variant IVS4–19G->A in the remaining allele. Four lines, including FTC-133, express PTEN mRNA at low levels. In general, PTEN protein levels correlated with mRNA levels, except for NPA87, which has low levels of transcript and relatively high levels of PTEN protein. Transient expression of PTEN in seven thyroid cancer cell lines resulted in G1 arrest in two well differentiated papillary thyroid cancer lines (PTCs) and both G1 arrest and cell death in the remaining five lines, including three FTCs, one poorly differentiated PTC and one undifferentiated thyroid cancer. The level of phosphorylated Akt was inversely correlated with the endogenous level of PTEN protein and overexpression of PTEN-blocked Akt phosphorylation in all cells analysed. Our results suggest that downregulation of PTEN expression at the mRNA level plays a role in PTEN inactivation in thyroid cancer and PTEN exerts its tumour-suppressive effect on thyroid cancer through the inhibition of cell cycle progression alone or both cell cycle progression and cell death.

+ To whom correspondence should be addressed at: Human Cancer Genetics Program, The Ohio State University, 420 West 12th Avenue, Suite 690 TMRF, Columbus, OH 43210, USA. Tel: +1 614 292 2347; Fax: +1 614 688 3582; Email: eng-1@medctr.osu.edu


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