Meningioma Drug Discovery Service

Meningioma is the most prevalent vascular-rich tumor in the central nervous system. Although meningioma is a benign tumor, it has a high recurrence rate after complete resection, which induces postoperative meningitis or neurologic deficits. Besides, the pathogenesis of meningioma is complex. Therefore, there is an urgent need to investigate the mechanisms of action in meningioma in order to explore novel targeting therapeutics that improve the patient's outcomes. With years of experience and sophisticated technologies, Creative Biolabs has the confidence in offering a wide range of solutions in the field of neuroscience. Our experts consolidate global resources and technologies, which enable researchers and developers to grasp the mechanisms of action in meningioma.

Mechanism of Action Studies of Meningioma

The mechanisms of action in meningioma are intimately related to chromosomal variations and alterations in multiple molecular signaling pathways. All or partial loss of chromosome 22 is the primary chromosomal abnormality in human meningioma. In addition, NF2 gene mutation and losses, gains, amplifications, and alterations of chromosomes are involved in the progression of meningioma from beginning meningioma to atypical and anaplastic meningioma. The molecular mechanisms involved in meningioma are complex, including dysregulation of cell growth and proliferation, increased cell invasiveness, angiogenesis, and inhibition of apoptosis.

1. The mammalian target of rapamycin (mTOR) is overactivated in meningioma primarily modulated by the phosphoinositide-3-kinase (PI3K)/protein kinase B (Akt) pathway. mTOR can further phosphorylate and activate S6K1 and 4EBP which affect gene expression, contributing to cell growth, proliferation, and tumorigenesis.

2. The low expression or absence of E-cadherin and enhanced matrix metalloproteinase 9 (MMP-9) lead to increased degradation of the extracellular matrix, which increases cell invasiveness. The deficiency of density-enhanced phosphatase-1 (DEP-1) seems to be related to the upregulation of MMP-9 levels. Reduced expression of A-kinase anchor protein 12 (AKAP12) inhibits intercellular adhesion and contact and promotes cell invasiveness.

3. Angiogenesis in meningioma is modulated by vascular endothelial growth factor (VEGF), which is regulated by JAK/STAT and PI3K/Akt signaling pathways as well as enhanced MMP-9 levels. Furthermore, the Wnt signaling pathway inhibits neural cell apoptosis.

Fig.1 Selected signaling pathways in meningiomas and molecular targets for drug therapy. (Qin, 2021)

Meningioma Solutions at Creative Biolabs

According to the mechanisms, potential agents targeting mTOR, phosphorylation of the PI3K/Akt pathway, VEGF, etc., can thus be developed as prospective treatment regimens for patients with meningioma. Creative Biolabs is committed to providing a wide range of discovery services to assist researchers in exploring novel targets and screening the corresponding therapeutics. In addition to targeting therapies, immunotherapy is also a promising treatment strategy used in meningioma. Our scientists assist researchers to design customized programs with a variety of in vitro, in vivo, and ex vivo assays using our sophisticated technologies and customized meningioma neuron culture, pathological sections, and tumor animal models. We help you to understand further molecular mechanisms involved in meningioma, which promotes research and development of both targeting therapeutics and immunotherapies. You can find more details about our platform and one-stop solution for translational research and integrated research in meningioma with the following scheme.

If you have the intention to learn more about preclinical meningioma drug discovery services, please feel free to contact us.

Reference

1. Qin, C.; et al. Brain-invasive meningiomas: Molecular mechanisms and potential therapeutic options. Brain Tumor Pathology. 2021, 38(3): 156-172.