Pharmacological Reports· 2026Q1· Review
DUSP6/MKP3 as an emerging therapeutic target in glioblastoma
- 1citations
- Q1SCImago
- 2026year
Short summary
DUSP6/MKP3, frequently overexpressed in glioblastoma (GBM), drives tumor growth, invasion, and treatment resistance, making it a promising therapeutic target for this aggressive brain cancer.
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Key points
- DUSP6/MKP3 is frequently overexpressed in glioblastoma (GBM).
- This phosphatase promotes GBM growth, invasive behavior, and treatment resistance.
- Computational analyses identify DUSP6/MKP3 as a dysregulated gene in GBM driver networks.
- DUSP6/MKP3 is emerging as a potential therapeutic target for glioblastoma.
AI-generated from the title and abstract; the full text is not read.
Abstract
The role of MKP family dual-specificity phosphatases (DUSPs) in oncogenesis, together with their potential as therapeutic targets in precision oncology, is now well established. These enzymes dephosphorylate both phosphotyrosine and phosphothreonine residues on extracellular signal-regulated kinase ERK1/2, thereby attenuating mitogen-activated protein kinase (MAPK) signalling. DUSP6/MKP3 acts as a context-dependent regulator with tumour-suppressive or tumour-promoting roles across cancers. Glioblastoma (GBM), an aggressive primary brain tumour with dismal clinical outcomes, has shown limited response to both oncogene-targeted and immunotherapeutic approaches. DUSP6/MKP3 is frequently overexpressed in GBM and contributes to tumour growth, invasive behaviour, and treatment resistance. Computational analyses identify DUSP family genes, including DUSP6/MKP3, as recurrently dysregulated within GBM driver networks, supporting a central role in gliomagenesis. Here, we discuss DUSP6/MKP3 in glioblastoma, integrating transcriptional and cell-based evidence to define its molecular mechanisms and clinical relevance.
The authors' abstract, as published at the source. Pharmacological Reports, 2026 · DOI ↗
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Field: Genetics (Medicine)
GeneticsMedicine