Bcl-2 loss rates were not significantly different between proliferative endometrium and benign hyperplasia (P = 0.12) and between premalignant hyperplasia and endometrial cancer (P = 0.53).
Nude mice with xenografted implants of human EC HEC-1-B cells were treated with valproic acid (VPA) and decitabine (DAC) and evaluated for tumor growth, CDH1 and Bcl-2 mRNA levels.
Bcl-2 mRNA and protein expression was increased in cisplatin-resistant endometrial cancer cell lines (KLE and HEC-1-A), but not in cisplatin-sensitive cell line (Ishikawa).
Except for ER, there must be other binding location of estrogen in endometrial cancer cells, and the nongenomic effects of estrogen initiated from plasma membrane by E2-BSA cannot lead to transcriptional effect of Bcl-2 expression.
Phenotypic and molecular variables (ploidy, proliferating cell nuclear antigen, MIB-1, p53, HER-2/neu, and bcl-2) were analyzed in preoperative specimens from 82 patients with endometrial cancer who had lymph nodes dissected.
Our results indicated that ursolic acid induced apoptotic processes in these poorly differentiated endometrial cancer cells occurs through mechanisms involving mitochondrial pathways and Bcl-2 family proteins.
To test this hypothesis, we treated endometrial cancer cells (Ishikawa cell line) with quercetin, and cell proliferation, expression of growth signal genes (EGF, VEGF, and TGF-alpha), cell cycle genes (p53, p21, p73, and cyclin D1), and apoptosis-related genes (bcl-2 and bax) were analyzed.