Year: 2025
Type: review
Abstract: Glioblastoma (GBM) is a highly aggressive brain tumor with limited treatment options and poor prognosis. Proline-rich tyrosine kinase 2 (Pyk2) has been implicated in regulation of GBM invasion, proliferation, and recurrence. Its activation, driven by tumor-infiltrating microglia and macrophage-derived extracellular factors such as EGF, PDGFB, SDF-1α, IL-6, and IL-8, enhances tumor cell motility and survival. Experimental studies demonstrate that pharmacological inhibition or genetic knockdown of Pyk2 significantly reduces glioma cell migration and proliferation. Furthermore, recurrent GBM tumors exhibit elevated Pyk2 phosphorylation in mouse GBM models, correlating with increased tumor growth. Inhibition of Pyk2 and the structurally related focal adhesion kinase (FAK) signaling has shown promising results in preclinical studies, reducing tumor recurrence and improving survival outcomes. This review summarizes recent findings and underscores the pivotal role of Pyk2 in GBM pathophysiology, highlighting its potential as a therapeutic target.
Source: Cancers
Authors: Lilia Kucheryavykh, Yuriy Kucheryavykh
Institution: Central University of the Caribbean
Language: English
Subfield: Genetics
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,499
OpenAlex ID: W4413225295