Hesperidin promotes programmed cell death by downregulation of nongenomic estrogen receptor signalling pathway in endometrial cancer cells.

摘要: Endometrial carcinoma (EC) is the most common malignant gynecologic tumor in women. EC thought to be caused by increasing estrogen levels relative progesterone body. Hesperidin (Hsd), a biologically active flavonoid, could extracted from Citrus species. It has been recently shown that Hsd exert anticarcinogenic properties different cancer types. However, effects of and its molecular mechanisms on remain unclear. In this study, antiproliferative, apoptotic genomic underlying were identified. We found significantly suppressed proliferation cells dose time dependent manner. Mechanistic studies showed contribute apoptosis inducing externalization phosphatidyl serine (PS), caspase-3 activity loss mitochondrial membrane (MMP). Furthermore, we examined also upregulate expression proapoptotic Bax subgroup genes (Bax Bik) while downregulating anti-apoptotic protein Bcl-2 cell lines. According GO enrichment KEGG pathway analysis differentially expressed treated cells, identified promote death via downregulation receptor I (ESRI) was directly related ERK/MAPK pathway. Taken together, our study first an antiestrogenic compound modulate nongenomic signaling through inhibition growth. Our findings may provide us novel growth inhibitory agent for treatment after verifying mechanism with vivo studies.