ArticleBiochemistry and biophysics reports2025
VH032 suppresses glioma proliferation by inhibiting the VHL/HIF-1α/VEGF pathway.
Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: VH032 is a VHL ligand employed for the recruitment of the von Hippel-Lindau (VHL) protein. Recent studies reveal VHL exhibits significant antitumour effects on various tumor cells. Nevertheless, VH032's impacts on glioma cells remain largely unexplored. Methods: The study explored VH032's impact on glioma cell lines U87MG and U251 through a series of experimental assessments. The experiments included cell viability assays, wound healing assays and transwell assays. The apoptotic activity of VH032 was determined via flow cytometry. Finally, a xenograft tumor model composed of nude mice was used to confirm the results. Results: In vitro, the CCK-8 assay indicated that VH032 potently inhibited the proliferation of glioma cells. Wound healing and transwell assays further revealed that the drug significantly impaired glioma cell migration and invasion. Flow cytometry analysis demonstrated an increased rate of apoptosis in the drug-treated cell population. Moreover, the inhibitory effect on the VHL/HIF-1α/VEGF signaling pathway was confirmed, supporting its role in reducing tumour growth. The xenograft mouse study confirmed that VH032 markedly inhibited tumour growth. Conclusion: These findings suggest that VH032 is a novel and promising chemotherapeutic agent for gliomas, acting through the interference of the VHL/HIF-1α/VEGF signaling pathway to suppress migration and invasion of glioma cells.
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