Wnt signalling pathways are highly significant protein substances within the body. They are responsible for passing signals across cell membrane receptors from without the cell to within the cell. This communication can occur either among neighbouring cells or within the same cell. The pathways play a regulatory role in that it regulates gene transcription, cytoskeleton, and calcium within the cell. Wnt signalling pathways are unique in that they are similar in several 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 signalling is activated aberrantly, it leads to poor prognosis of various cancers such as ovarian and breast cancer. The pathways may also lead to cancer formation due to de-regulation. This paper analyses the role of wnt signalling in the development of breast and ovarian cancer in order to understand how wnt regulation may contribute to cancer therapy.
There are three main types of Wnt pathways. These include canonical, 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 Frizzled Receptor Proteins (SFRP 1-5) are good examples of the Wnt antagonists. SFRP 4 deactivation is especially associated with development of ovarian and breast cancer since it is often deposited into the blood stream giving room for the action of Wnt proteins. Patients who lack SFRP4 express faster cancer progression because of lack of proper wnt regulation.
Stem cell and stem-like cells ...
... middle of paper ...
...nclude SFRP 1-5. Introducing these regulators in the cell leads to lower cancer progression due to the ability to moderate wnt and reduce beta catenin production.
The studies analysed herein indicate that Wnt regulation is impaired in cancer cells. This implies that resistance to current cancer therapies is associated with this anomaly. Lack of Wnt regulation also leads to increases in beta catenin, which leads to enhanced migration of cancer cells. However, the studies do not offer the way forward for cancer treatment options. There is need to use these findings to create recombinant Wnt antagonists such as SFRP4 in order to reduce cancer progression, reduce migration of cancer cells, and enhance adherence of cancer cells. There is also need for an in-depth study of Wnt ligands to enhance specificity between the ligands and the Wnt antagonists.
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