Introduction Wnt signaling pathways are highly significant protein substances within the body. They are responsible for passing signals through cell membrane receptors from outside the cell to inside the cell. This communication can occur both between neighboring cells and within the same cell. The pathways play a regulatory role as they regulate gene transcription, the cytoskeleton, and calcium within the cell. Wnt signaling pathways are unique in that they are similar in different species. The pathways are also associated with embryonic development and carcinogenesis. They regulate processes such as cell migration, proliferation and cell fate specification. When wnt signaling is abnormally activated, it leads to a poor prognosis of various cancers such as ovarian and breast cancer. The pathways can also lead to tumor formation due to deregulation. This article analyzes the role of wnt signaling in the development of breast and ovarian cancer in order to understand how wnt regulation may contribute to cancer therapy. Background Information There are three main types of Wnt pathways. These include canonical and non-canonical pathways depending on their dependence on beta catenin. Canonical pathways depend on beta catenin while non-canonical pathways do not. Research shows that Wnt antagonists are often deactivated in cancer patients. Secreted frizzle receptor proteins (SFRP 1-5) are good examples of Wnt antagonists. Deactivation of SFRP 4 is particularly associated with the development of ovarian and breast cancer as it often settles in the bloodstream giving way to the action of Wnt proteins. Patients lacking SFRP4 express faster cancer progression due to lack of adequate wnt regulation. Stem Cells and Stem Cells ... middle of paper ...... include SFRP 1-5. Introducing these regulators into the cell leads to less cancer progression due to the ability to moderate Wnt and reduce beta catenin production. Recommendation: The studies analyzed here indicate that Wnt regulation is impaired in cancer cells. This implies that resistance to current anticancer therapies is associated with this anomaly. Lack of Wnt regulation also leads to increased beta catenin, which leads to increased tumor cell migration. However, the studies do not offer the way forward for cancer treatment options. It is necessary to use these findings to create recombinant Wnt antagonists such as SFRP4 in order to reduce cancer progression, reduce tumor cell migration, and improve tumor cell adhesion. An in-depth study of Wnt ligands is also needed to improve specificity between Wnt ligands and antagonists.