ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2024
[Role of Notch 1 signaling and glycolysis in the pathogenic mechanism of adenomyosis].
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Pathogenesis of Adenomyosis: An Integrated Review of Cellular Origins, Molecular Mechanisms, and Intersecting Diseases.Journal of cellular and molecular medicine · 2026Review
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5 authors.
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Abstract
objectiveTo investigate the expressions of glycolysis-related factors and changes in Notch1 signaling in endometrial tissues of adenomyosis (AM) and Ishikawa cells to explore the pathogenesis of AM.
methodsEutopic endometrial tissues were collected from 8 patients with AM and 8 patients with uterine fibroids matched for clinical characteristics (control group). The expressions of Notch1 signaling proteins and glycolysis-related factors in the collected tissues were detected using qRT-PCR and Western blotting, and the levels of glucose and lactic acid were determined. An Ishikawa cell model with lentivirus-mediated stable Notch1 overexpression was established for assessing cell survival rate with CCK-8 assay, cell migration and invasion abilities with Transwell migration and invasion assays, and glycolytic capacity by determining the extracellular acidification rate.
resultsCompared with those in the control group, the endometrial tissues in AM group showed significantly increased expression level of carbohydrate antigen 125 (CA125), increased mRNA expression levels of Notch1, HK2 and PDHA and protein expressions of Notch1, GLUT1, HK2, PKM and PDHA, lowered glucose level and increased lactate level. The Ishikawa cell models with stable Notch1 overexpression exhibited significantly increased cell survival rate with attenuated cell migration and invasion abilities and decreased glycolysis capacity and reserve.
conclusionThe Notch1 signaling pathway participates in the pathogenesis of AM possibly by regulating the proliferation, migration, invasion and glycolysis of endometrial cells.
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