Hirudin suppresses ovarian cancer cell proliferation and glycolysis through inhibiting the NF-B/HK3 axis
Research article published in Gene (2026)
Abstract
BACKGROUND: Ovarian cancer (OC) is a highly lethal malignancy, and chemoresistance remains a major obstacle to effective treatment. This study aims to investigate the therapeutic mechanisms of hirudin in OC, with the goal of identifying novel strategies to overcome chemoresistance. METHODS: The CCK8 assay was used to assess the viability of OC cells treatment with various concentrations of hirudin. Colony formation assays were conducted to evaluate cell proliferation, while wound healing and Transwell assays were used to examine cell migration and invasion, respectively. To investigate the potential molecular mechanisms underlying hirudin's effects on OC, network pharmacology analysis was performed by integrating data from SuperPred, TargetNet, GeneCards, OMIM, and DisGeNET to identify candidate target genes associated with both hirudin and OC. Importantly, dual-luciferase reporter assays were carried out to further evaluate the regulatory effects of hirudin on the transcriptional activity of key target genes. RESULTS: We found that hirudin inhibits the proliferation, migration, and invasion of OC cells in a concentration-dependent manner. Network pharmacology analysis identified nuclear factor-κB (NF-κB) as a potential key molecular target of hirudin. Mechanistically, hirudin suppresses glycolytic activity by inhibiting NF-κB to downregulate Hexokinase 3 (HK3) expression in OC cells. Consequently, both the extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were significantly reduced. CONCLUSION: This study provides a theoretical foundation for elucidating the molecular mechanisms underlying the anti-tumor effects of hirudin in OC and suggests its potential as a candidate for metabolism-targeted therapy.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Zusammenfassung
Ovarian cancer (OC) is a highly lethal malignancy, and chemoresistance remains a major obstacle to effective treatment.
Warum dies für die Hirudotherapie relevant ist
This study investigated hirudin's effects on ovarian cancer (OC) cells, assessing viability, proliferation, migration, and invasion using CCK8, colony formation, wound healing, and Transwell assays, along with network pharmacology and dual-luciferase reporter analyses. The results showed that hirudin concentration-dependently inhibits OC cell proliferation, migration, and invasion by suppressing NF-κB-mediated HK3 expression, thereby reducing glycolytic activity (ECAR and OCR). While hirudin is examined here as a potential anti-tumor agent, the abstract provides no information about leeches, leech saliva, or hirudotherapy, so any connection to the leech secretome cannot be drawn from this source. The findings are limited to in vitro cell-based experiments without in vivo validation or clinical data, and no leech-related context is mentioned.
Zitation
Hirudin suppresses ovarian cancer cell proliferation and glycolysis through inhibiting the NF-B/HK3 axis
Guo Y et al. · Gene, 2026
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