Mitogen-activated protein kinases (MAPKs) are a group of serine/threonine kinases which are activated in response to a diverse array of extracellular stimuli, and mediate signal transduction from the cell surface to the nucleus. The chemotherapeutic agents, growth factors and reproductive hormones have been demonstrated to activate MAPKs, suggesting that the MAPK signaling pathway plays an important role in the regulation of proliferation, apoptosis, survival and differentiation in response to these external stimuli in ovarian cancer. In addition to MAPKs as an oncogenic pathway, phosphatidylinositol 3-kinase (PI3K) plays a role in a various range of important cellular processes associated with malignant characterestics including cell growth, survival and migration, which is a member of lipid kinases subfamily that phosphorylates and dephosphorylates the 3-position of the inositol ring of phosphoinositides in a membrane. In this review, recent results of the MAPK and PI3K signaling cascades by external stimuli, and potential roles of these oncogenic pathways as an oncogenic pathway are summarized in epithelial ovarian cancer.