Immunhistochemistry profiling of human endometrial cancer tissue biopsies identified epithelial cells co-expressing ERβ5 and ERα in stage I endometrial adenocarcinomas and post menopausal endometrium.
Estrogen receptor (ER), progesterone receptor (PR), and Ki-67 and P53 receptor levels in endometrial curettage material were investigated for their ability to predict lymph node (LN) involvement in patients with endometrioid-type endometrial cancer (EEC).
Notably, InsR-β inhibition had a limited effect on estradiol-dependent proliferation, cell cycle, and apoptosis, whereas ER-α inhibition had a limited insulin-dependent effect, in EC cell lines.
Conditioned medium from selective ERα agonist-treated M2 macrophages induced the epithelial to mesenchymal transition (EMT) in endometrial cancer cells.
To assess the effect of skincare product use on the risk of pre- and postmenopausal breast cancer, estrogen receptor positive (ER+) and negative (ER-) breast cancer and cancer of the endometrium.
Compared to that of the general population, the incidence of EC following estrogen receptor-positive (ER+) breast cancer and hormone receptor-negative (HR-) breast cancer increased by approximately 16-fold and 15-fold, respectively.
Proline-, glutamic acid-, and leucine-rich protein-1 (PELP1), a co-regulatory molecule of estrogen receptor α (ER α), is up-regulated in series of cancers such as endometrial carcinoma, ovarian cancer, colorectal cancer, breast cancer, and non-small cell lung cancer.
The aim of this retrospective study was to explore the possible correlation in the EC microenvironment between master regulators of complex phenomena such as steroid responsiveness through estrogen receptor alpha (ERα) and progesterone receptor (PR), epithelial-to-mesenchymal transition (supported by SLUG transcription factor), hypoxia (with hypoxia inducible factor-1 alpha, HIF-1α), and obesity that has been recognized as a EC risk factor.
Using a unique CRISPR/Cas9 strategy, we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus.
Immunohistochemistry revealed an overexpression of phospho-NPM/B23 (Thr199) in human endometrial cancer, and phospho-NPM/B23 (Thr199) expression levels were inversely associated with Erα in clinical specimen.
Despite a high proportion of endometrioid ECs being ER and/or PR positive, endocrine therapy is only effective in a minority of women with EC and ultimately patients progress with resistance developing to treatment.
A20 increased functional ERα protein levels and enhanced estrogen-driven EC cell proliferation through preventing ERα protein degradation by its deubiquitinase activity.
HEC-1A and KLE, ERα-negative endometrial cancer cells exhibiting high ERRα expression levels, and HEC-1A cell-derived xenograft model mice were treated with XCT790.
Overall, Efp would exert a tumor-promoting role through modulating NF-κB pathway and 14-3-3σ protein degradation in endometrial cancer regardless of its estrogen receptor status.
Taken together, our study first showed that Hsd could be an antiestrogenic compound that could modulate nongenomic estrogen receptor signaling through inhibition of EC cell growth.
A total of 43 high-grade endometrial carcinoma cases initially classified as pure high-grade endometrioid carcinoma (n=32), mixed high-grade endometrioid carcinoma/serous carcinoma (n=9) and mixed high-grade endometrioid carcinoma/clear cell carcinoma (n=2) were retrospectively stained with a panel of immunostains, including antibodies for p53, p16, estrogen receptor, and mammaglobin.
Thus, our goal was to assess the effect of the isoflavones, novasoy and genistein, on cell proliferation, cell cycle, apoptosis, progesterone receptor (PR) and estrogen receptor-alpha (ERα) expression and the AKT/mTOR and MAPK pathways in endometrial cancer cells.
The mRNA and protein expression levels of ERRα and estrogen receptor α (ERα) were detected by qPCR and Western blotting in RL-952, AN3-CA, HEC-1A, and HEC-1B EC cell lines.