2. Academic Validation
  3. PFKFB3 promotes endometriosis cell proliferation via enhancing the protein stability of β-catenin

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

  • Mol Cell Endocrinol. 2023 Oct 9:112083. doi: 10.1016/j.mce.2023.112083.
Xi Ling 1,  Lan Liu 1,  Aifang Jiang 2,  Xiaodan Shi 3,  Lu Liu 1,  Xiaoyun Wang 1,  Chao Lu 2,  Chune Ren 4,  Zhenhai Yu 5
Affiliations

Affiliations

  • 1 Department of Reproductive Medicine, Affiliated Hospital of Weifang Medical University, Weifang, Shandong Province, PR China; School of Clinical Medicine, Weifang Medical University, Weifang, Shandong Province, PR China.
  • 2 Department of Reproductive Medicine, Affiliated Hospital of Weifang Medical University, Weifang, Shandong Province, PR China.
  • 3 Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, PR China.
  • 4 Department of Reproductive Medicine, Affiliated Hospital of Weifang Medical University, Weifang, Shandong Province, PR China. Electronic address: [email protected].
  • 5 Department of Reproductive Medicine, Affiliated Hospital of Weifang Medical University, Weifang, Shandong Province, PR China. Electronic address: [email protected].
PMID: 37820851 DOI: 10.1016/j.mce.2023.112083
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.

Keywords

Endometriosis; Epithelial-mesenchymal transition; PFK-015; PFKFB3; β-catenin.

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