The following is a summary of “PFKFB3 promotes endometriosis cell proliferation via enhancing the protein stability of β-catenin,” published in the December 2023 issue of Endocrinology by Ling, et al.
The inflammatory illness known as endometriosis is an extremely prevalent condition that affects women of reproductive age and is strongly linked to infertility. On the other hand, the molecular mechanism of endometriosis still needs to be better understood. PFKFB3, also known as 6-phosphofructose-2-kinase/fructose-2,6-bisphosphatase 3, is an enzyme that is essential to the process of glycolysis and an enzyme that plays a significant regulatory function in the development of cancer.
In the study, researchers discovered that endometriotic tissues had a high level of expression of PFKFB3. There is evidence that PFKFB3 promotes the formation and multiplication of endometriosis cells. Meanwhile, PFKFB3 promotes glycolysis in cells that are associated with endometriosis. Additionally, PFKFB3 encourages the migration and invasion of cells associated with endometriosis. Therefore, they concluded that PFKFB3 is responsible for the epithelial-mesenchymal transition (EMT) in endometriosis cells.
Through its interaction with β-catenin, an important factor in epithelial-mesenchymal transition (EMT), PFKFB3 enhances the protein stability of β-catenin. In addition, the PFKFB3 inhibitor PFK-015 can stunt the development of endometrial tissue and the formation of cells associated with endometriosis. In conclusion, their research findings indicate that PFKFB3 plays a significant part in the progression of endometriosis and provides novel concepts for the clinical diagnosis or therapy of endometriosis.
Source: sciencedirect.com/science/article/abs/pii/S0303720723002344
