PGK1 mediates glycolysis and cell proliferation in endometriosis by regulating DDIT4 nuclear translocation

Xuemei Zhang, Yadi Wang, Yujie Tang, Ran Wei, Runze Zhao, Zhenhai Yu, Chao Lü, Chao Lu
Biochimica et biophysica acta. Molecular cell research · 2025 · vol. 1872(7) , pp. 120009 · doi:10.1016/j.bbamcr.2025.120009 · PMID:40532826 · W4411347916
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⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

This study found that PGK1 promotes glycolysis and cell proliferation in endometriosis by controlling the nuclear translocation of DDIT4.

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Abstract

Endometriosis (EM), a gynecologic disorder affecting 10 % of childbearing age women, with complex pathogenesis involving cell proliferation and metabolic abnormalities similar to malignancies. Unusual expression of key enzymes and regulators in glycolysis pathway contributes to the development of endometriosis. Phosphoglycerate kinase 1 (PGK1) was a key enzyme in glycolysis with additional roles as a transcription factor co-activator and protein kinase. We discovered that PGK1 was elevated and associated strongly with the development of EM. The PGK1 inhibitor NG52 inhibited the growth of endometriosis lesions in mice by preventing cell migration and proliferation. Furthermore, we found that DNA damage response 4 (DDIT4) was a new downstream target gene of PGK1. PGK1 regulated the nuclear translocation of DDIT4. Additionally, we also observed that PGK1 up-regulate the transcriptional activity of DDIT4, leading to DDIT4 overexpression that promoted the development of endometriosis. These findings may provide new insights for potential non-hormonal targeted therapies for endometriosis treatment.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (54)

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