PFKFB3 promotes endometriosis cell proliferation via enhancing the protein stability of β-catenin.

Abstract

Endometriosis is a common inflammatory disease in women of reproductive age and is highly associated with infertility. However, the molecular mechanism of endometriosis remains unclear. 6-Phosphofructose-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) is a key enzyme in glycolysis and plays an important regulatory role in the development of cancer. Here we found that PFKFB3 is highly expressed in endometriotic tissues. PFKFB3 promotes the proliferation and growth of endometriosis cells. Meanwhile, PFKFB3 promotes glycolysis in endometriosis cells. Furthermore, PFKFB3 promotes migration and invasion of endometriosis cells. On this basis, we found that PFKFB3 promotes epithelial-mesenchymal transition (EMT) in endometriosis cells. PFKFB3 interacts with the essential factor of EMT, β-catenin, and promotes the protein stability of β-catenin. In addition, the PFKFB3 inhibitor PFK-015 inhibites the growth of endometriosis cells and the development of endometrial tissue. In conclusion, our study shows that PFKFB3 plays an important role in the development of endometriosis and provides new ideas for the clinical diagnosis or treatment of endometriosis.

• Authors: Xi Ling, Lan Liu, Aifang Jiang, Xiaodan Shi, Lu Liu, Xiaoyun Wang, Chao Lu, Chune Ren, Zhenhai Yu
• Journal: Molecular and cellular endocrinology (Mol Cell Endocrinol) Vol. 579 Pg. 112083 (Jan 01 2024) ISSN: 1872-8057 [Electronic] Ireland
• PMID: 37820851 (Publication Type: Journal Article)
• Copyright: Copyright © 2023 Elsevier B.V. All rights reserved.

Chemical References

• beta Catenin
• PFKFB3 protein, human
• Phosphofructokinase-2
• CTNNB1 protein, human

Topics

• Female
• Humans
• beta Catenin (metabolism)
• Cell Proliferation
• Cells, Cultured
• Endometriosis (genetics, metabolism)
• Epithelial-Mesenchymal Transition
• Phosphofructokinase-2 (genetics, metabolism)
• Protein Stability