PFKFB3 promotes endometriosis cell proliferation via enhancing the protein stability of β-catenin
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PFKFB3 increases endometriosis cell proliferation by stabilizing the protein levels of β-catenin.
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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.
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Cited by (5)
- Glycolytic reprogramming in endometriosis: molecular mechanisms, immune modulation, and non-hormonal therapeutic opportunities 2026
- Metabolic reprogramming in endometriosis: mechanisms and therapeutic prospects 2026
- Warburg-like Metabolic Reprogramming in Endometriosis: From Molecular Mechanisms to Therapeutic Approaches 2025
- AARS1 promotes endometriosis progression by promoting the lactylation of Snail1† 2025
- The role of somatic mutations in endometriosis: pathogenesis, progression, and fibrogenesis (narrative review) 2025
Source provenance
- europepmc
- last seen: 2026-07-26T06:08:39.051465+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-07-26T06:07:14.836930+00:00
- unpaywall
- last seen: 2026-06-02T02:00:03.124865+00:00
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