Rapid estrogen signaling negatively regulates PTEN activity through phosphorylation in endometrial cancer cells.

ABSTRACT: 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 on normal and malignant endometrium 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/AKT signaling axis. PTEN levels are elevated during the E2 dominated, mitotically active, proliferative phase of the menstrual cycle, indicating possible hormonal regulation of PTEN in the uterus. In order to determine if rapid E2 signaling regulates PTEN, we used ERα-positive, PTEN-positive, endometrial

SUBMITTER: Scully MM 

PROVIDER: S-EPMC4103875 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature