ReviewFrontiers in oncology2026
The role of MELK in cancer: mechanisms and therapeutic options.
Review in Frontiers in oncology, 2026. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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9 authors.
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Abstract
Cells undergo tight regulation during the mitotic phase of the cell cycle, which produces genetically identical daughter cells and prevents the segregation of duplicate chromosomes. This regulatory network has identified maternal embryonic leucine zipper kinase (MELK) as a proliferation-associated regulator. MELK is highly expressed in actively dividing cells and is often overexpressed in multiple human cancers. Beyond its canonical role in mitotic regulation, MELK is implicated in numerous oncogenic processes, including transcriptional and epigenetic regulation, inflammation, epithelial-mesenchymal transition (EMT), DNA damage response (DDR), and treatment resistance. Even though pharmacological inhibition of MELK has shown encouraging anticancer effects in preclinical models, its biological requirement remains context-dependent and poorly understood. By integrating mechanistic insights with translational and clinical evidence, this review offers a comprehensive perspective on MELK that stands out in the existing literature for its critical evaluation of context-dependent functions and therapeutic relevance. We highlight key gaps that must be addressed to establish MELK as a reliable cancer biomarker and therapeutic target.
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