Changes in EndometrialPTENExpression throughout the Human Menstrual Cycle1

George L. Mutter, Ming-Chieh Lin, Jeffrey T. Fitzgerald, Jennifer B. Kum, Charis Eng
In: The Journal of Clinical Endocrinology & Metabolism · 2000 · vol. 85(6) , pp. 2334–2338 · doi:10.1210/jcem.85.6.6652 · PMID:10852473 · W2031187395
article OA: bronze CC0 ⤵ 15 in-corpus citations
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This study examined PTEN expression in human endometrium during the menstrual cycle and found that PTEN RNA and protein levels change dynamically in epithelial and stromal cells in response to estrogen and progesterone.

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Abstract

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.

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