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.
Resumen
Ovarian cancer (OC) is a highly lethal malignancy, and chemoresistance remains a major obstacle to effective treatment.
Por qué esto importa para la hirudoterapia
Este estudio investigó los efectos de la hirudina sobre células de cáncer de ovario (OC), evaluando viabilidad, proliferación, migración e invasión mediante ensayos de CCK8, formación de colonias, cicatrización de heridas y Transwell, junto con farmacología de red y análisis de doble luciferasa reportero. Los resultados mostraron que la hirudina inhibe de forma dependiente de la concentración la proliferación, migración e invasión de células de OC, mediante la supresión de la expresión de HK3 mediada por NF-κB, reduciendo así la actividad glucolítica (ECAR y OCR). Si bien la hirudina se examina aquí como un potencial agente antitumoral, el resumen no proporciona información sobre sanguijuelas, saliva de sanguijuela ni hirudoterapia, por lo que cualquier conexión con el secretoma de la sanguijuela no puede establecerse a partir de esta fuente. Los hallazgos se limitan a experimentos in vitro basados en líneas celulares sin validación in vivo ni datos clínicos, y no se menciona ningún contexto relacionado con la sanguijuela.
Citación
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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Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: 18 de junio de 2026