Icariside II Suppresses the Malignant Behaviors of Breast Cancer Cells by Inhibiting PTGES3 Expression

Here, we aimed to explore the roles of prostaglandin E synthase 3 in breast cancer and assess whether icariside II inhibits breast cancer by modulating prostaglandin E synthase 3 expression. Prostaglandin E synthase 3 levels were determined via immunohistochemistry and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) in breast cancer tissues and western blotting and qRT-PCR in breast cancer cells. Cell growth and apoptosis were assessed via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry assays. Caspase 3 activity was measured using the caspase 3 measuring kit. Migration and invasion of cancer cells were analyzed via transwell assay. Moreover, related protein levels were determined via western blotting. Icariside II inhibited the proliferation, migration, and invasion and induced the apoptosis of breast cancer cells. Icariside II also decreased prostaglandin E synthase 3 levels in breast cancer cells. Prostaglandin E synthase 3 levels were elevated in breast cancer tissues and cells. Prostaglandin E synthase 3 silencing significantly inhibited proliferation, induced apoptosis, and increased caspase 3 activity in breast cancer cells. It also decreased the protein levels of proliferating cell nuclear antigen and B cell lymphoma-2 and increased those of Bcl-2-associated X (Bax). Prostaglandin E synthase 3-siRNA inhibited cell migration and invasion and decreased the protein levels of matrix metalloproteinase-2 and -9. Overall, prostaglandin E synthase 3 was overexpressed in breast cancer. Its silencing inhibited the proliferation, migration, and invasion and induced the apoptosis of breast cancer cells. Furthermore, icariside II suppressed breast cancer progression by inhibiting prostaglandin E synthase 3 expression.