Related Experiment Video
Updated: Jan 8, 2026

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
Published on: July 10, 2019
Hirudin inhibits cell growth via ERK/MAPK signaling in human glioma
1Department of Gastroenterology, The First People's Hospital of Yuhang Hangzhou 310016, Zhejiang, P. R. China.
Abstract:
Glioma is one of the most common intracranial tumors, and the prognosis is poor though more and more treatments are employed. ERK/MAPK signaling has been reported to be associated with glioma. In the present study, we aimed to investigate hirudin as an antineoplastic drug inhibits ERK/MAPK signaling in glioma growth in vitro. The cell proliferation and apoptosis rate were detected using MTS and Annexin V staining assay, cell cycle distribution was detected using flowcytometry assay. Furthermore, the relevant molecules of ERK/MAPK signaling were examined using Western blot analysis and immunofluorescence staining assay. We provide the first evidence that hirudin increase inactivation state of ERK1/2, down-regulate the expression of canonical ERK/MAPK signaling pathway and establish an important role for hirudin in the treatment of glioma cells.
Insights
Hirudin, a potential glioma treatment, inhibits ERK/MAPK signaling pathways. This study shows hirudin increases ERK1/2 inactivation, reducing glioma cell growth and promoting apoptosis.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Pharmacology
Background:
- Glioma is a common and aggressive brain tumor with poor prognosis.
- The Extracellular signal-Regulated Kinase/Mitogen-Activated Protein Kinase (ERK/MAPK) signaling pathway is implicated in glioma development.
- Existing treatments for glioma have limited efficacy, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the potential of hirudin as an antineoplastic agent against glioma.
- To determine if hirudin inhibits the ERK/MAPK signaling pathway in glioma cells.
- To evaluate the effects of hirudin on glioma cell proliferation, apoptosis, and cell cycle progression.
Main Methods:
- In vitro study using glioma cell lines.
- Cell proliferation assessed by MTS assay.
- Apoptosis detected using Annexin V staining.
- Cell cycle distribution analyzed by flow cytometry.
- ERK/MAPK signaling pathway molecules examined via Western blot and immunofluorescence.
Main Results:
- Hirudin treatment led to increased inactivation of ERK1/2.
- Down-regulation of the canonical ERK/MAPK signaling pathway was observed.
- Hirudin significantly affected glioma cell proliferation and apoptosis rates.
- Changes in cell cycle distribution were noted following hirudin treatment.
Conclusions:
- Hirudin demonstrates antineoplastic effects on glioma cells in vitro.
- Hirudin inhibits glioma growth by modulating the ERK/MAPK signaling pathway.
- Hirudin represents a promising therapeutic candidate for glioma treatment.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
Inhibition of Cdk Activity
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
MAPK Signaling Cascades
Mitogens and the Cell Cycle

