Document Detail

Changes in endometrial PTEN expression throughout the human menstrual cycle.
MedLine Citation:
PMID:  10852473     Owner:  NLM     Status:  MEDLINE    
Frequent mutation of the PTEN tumor suppressor gene in endometrial adenocarcinoma has led to the prediction that its product, a phosphatase that regulates the cell cycle, apoptosis, and possibly cell adhesion, is functionally active within normal endometrial tissues. We examined PTEN expression in normal human endometrium during response to changing physiological levels of steroid hormones. PTEN ribonucleic acid levels, assessed by RT-PCR, increase severalfold in secretory compared to proliferative endometrium. This suggested that progesterone, a known antineoplastic factor for endometrial adenocarcinoma, increases PTEN levels. Immunohistochemistry with an anti-PTEN monoclonal antibody displayed a complex pattern of coordinate stromal and epithelial expression. Early in the menstrual cycle under the dominant influence of estrogens, the proliferative endometrium shows ubiquitous cytoplasmic and nuclear PTEN expression. After 3-4 days of progesterone exposure, glandular epithelium of early secretory endometrium maintains cytoplasmic PTEN protein in an apical distribution offset by expanding PTEN-free basal secretory vacuoles. By the midsecretory phase, epithelial PTEN is exhausted, but increases dramatically in the cytoplasm of stromal cells undergoing decidual change. We conclude that stromal and epithelial compartments contribute to the hormone-driven changes in endometrial PTEN expression and infer that abnormal hormonal conditions may, in turn, disrupt normal patterns of PTEN expression in this tissue.
G L Mutter; M C Lin; J T Fitzgerald; J B Kum; C Eng
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  85     ISSN:  0021-972X     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-06-23     Completed Date:  2000-06-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2334-8     Citation Subset:  AIM; IM    
Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
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MeSH Terms
Endometrium / metabolism*,  pathology
Epithelial Cells / metabolism,  pathology
Gene Expression Regulation*
Genes, Tumor Suppressor*
Menstrual Cycle / metabolism*
PTEN Phosphohydrolase
Phosphoric Monoester Hydrolases / analysis,  genetics*
Reverse Transcriptase Polymerase Chain Reaction
Stromal Cells / metabolism,  pathology
Tumor Suppressor Proteins*
Uterine Diseases / genetics,  surgery
Grant Support
Reg. No./Substance:
0/Tumor Suppressor Proteins; EC 3.1.3.-/Phosphoric Monoester Hydrolases; EC protein, human; EC Phosphohydrolase

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