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Objective: To evaluate the clinical and pathological features of endometrial cancer (EC) following breast cancer and to assess the effect of the breast cancer hormone receptor status on subsequent EC. Materials: A retrospective study based on SEER data of EC patients with a history of breast cancer. Results: A total of 2142 cases met the inclusion criteria. 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. Histologically, the proportions of type II EC following ER+ breast cancer, HR− breast cancer and primary EC were 39.6%, 39.4% and 31.2%, respectively (P < 0.001). The proportions of G3 ECs were 26.9%, 28.2% and 19.8%, respectively (P < 0.001). The proportion of patients who died from miscellaneous malignant tumors among EC patients following breast cancer was significantly higher than the proportion of patients among primary ECs. The overall survival rate was worse for EC patients with a history of breast cancer (P < 0.001). There were no significant differences between patients with EC following ER+ breast cancer and those with EC following HR− breast cancer with regard to stage, lymphatic metastasis, outcome or cause of death. Conclusions: Compared to the general population, the incidence of EC in patients with breast cancer was increased markedly. Patients with EC following ER+ or HR− breast cancer shared the same clinicopathological features and prognoses. All patients need close monitoring regardless of breast cancer hormone receptor status. [ABSTRACT FROM AUTHOR]

Epithelial ovarian cancer (EOC) has the highest mortality among various types of gynecological malignancies. Most patients die of metastasis and recurrence due to cisplatin resistance. Thus, it is urgent to develop novel therapies to cure this disease. CCK-8 assay showed that nigericin exhibited strong cytotoxicity on A2780 and SKOV3 cell lines. Flow cytometry indicated that nigericin could induce cell cycle arrest at G0/G1 phase and promote cell apoptosis. Boyden chamber assay revealed that nigericin could inhibit migration and invasion in a dose-dependent manner by suppressing epithelial-mesenchymal transition (EMT) in EOC cells. These effects were mediated, at least partly, by the Wnt/β-catenin signaling pathway. Our results demonstrated that nigericin could inhibit EMT during cell invasion and metastasis through the canonical Wnt/β-catenin signaling pathway. Nigericin may prove to be a novel therapeutic strategy that is effective in patients with metastatic EOC. [ABSTRACT FROM AUTHOR]