Rapid estrogen signaling regulates PTEN: implications for cancer risk in steroid responsive tissues
Hyperestrogenicity is a risk factor for endometrial cancer. 17β-estradiol (E2) is known to stimulate both genomic and nongenomic estrogen receptor-α (ERα) actions in a number of reproductive tissues. However, the contributions of transcription-independent ERα signaling to normal and malignant endometrium and other steroid responsive cells are not fully understood. Phosphatase and tensin homolog (PTEN) is a tumor suppressor that decreases cellular mitosis primarily through negative regulation of the phosphoinositide 3-kinase (PI3K)/AKT signaling axis. PTEN levels are elevated during the E2 ...
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