Recombinant hirudin suppresses angiogenesis of diffuselarge B-cell lymphoma through regulation of the PAR-1-VEGF
Research article published in Chemical biology & drug design (2024)
Abstract
Hirudin is one of the specific inhibitors of thrombin, which has been confirmed to have strong bioactivities, including inhibiting tumors. However, the function and mechanism of hirudin and protease-activated receptor 1 (PAR-1) in diffuse large B-cell lymphoma (DLBCL) have not been clear. Detecting the expression PAR-1 in DLBCL tissues and cells by RT-qPCR and IHC. Transfected sh-NC, sh-PAR-1, or pcDNA3.1-PAR-1 in DLBCL cells or processed DLBCL cells through added thrombin, Vorapaxar, Recombinant hirudin (RH), or Na2S2O4 and co-culture with EA.hy926. And built DLBCL mice observed tumor growth. Detecting the expression of related genes by RT-qPCR, Western blot, IHC, and immunofluorescence, measured the cellular hypoxia with Hypoxyprobe-1 Kit, and estimated the cell inflammatory factors, proliferation, migration, invasion, and apoptosis by ELISA, CCK-8, flow cytometry, wound-healing and Transwell. Co-immunoprecipitation and pull-down measurement were used to verify the relationship. PAR-1 was highly expressed in DLBCL tissues and cells, especially in SUDHL2. Na2S2O4 induced SUDHL2 hypoxia, and PAR-1 did not influence thrombin-activated hypoxia. PAR-1 could promote SUDHL2 proliferation, migration, and invasion, and it was unrelated to cellular hypoxia. PAR-1 promoted proliferation, migration, and angiogenesis of EA.hy926 or SUDHL2 through up-regulation vascular endothelial growth factor (VEGF). RH inhibited tumor growth, cell proliferation, and migration, promoted apoptosis of DLBCL, and inhibited angiogenesis by down-regulating PAR-1-VEGF. RH inhibits proliferation, migration, and angiogenesis of DLBCL cells by down-regulating PAR-1-VEGF.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Resumen
Hirudin is one of the specific inhibitors of thrombin, which has been confirmed to have strong bioactivities, including inhibiting tumors.
Por qué esto importa para la hirudoterapia
Este estudio investigó la hirudina recombinante (RH), descrita como uno de los inhibidores específicos de la trombina, por sus efectos sobre el linfoma difuso de células B grandes (DLBCL) utilizando líneas celulares y modelos en ratón. La RH inhibió el crecimiento tumoral, la proliferación celular, la migración y la angiogénesis, al tiempo que promovió la apoptosis, con un mecanismo que involucra la regulación a la baja del eje de señalización PAR-1–VEGF. Esto es relevante para el ámbito de la ASH, ya que explora efectos terapéuticos de la hirudina, un inhibidor de la trombina, en un contexto oncológico. Advertencia: Se trata de un estudio preclínico que utiliza hirudina recombinante (un producto farmacéutico); no se involucra terapia con sanguijuelas ni material derivado de sanguijuelas, y los hallazgos requieren validación clínica antes de cualquier aplicación terapéutica.
Citación
Recombinant hirudin suppresses angiogenesis of diffuselarge B-cell lymphoma through regulation of the PAR-1-VEGF
Zhao J et al. · Chemical biology & drug design, 2024
Contexto clínico relacionado
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Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: 18 de junio de 2026