ArticleFrontiers in immunology2026
KDM5C-regulated SIX5 promotes glioblastoma progression through transcriptional activation of UBE2C and enhancement of the Warburg effect.
Article in Frontiers in immunology, 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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Abstract
Gliomas are the most common primary malignant tumors of the adult central nervous system, characterized by rapid growth, high recurrence rates, and limited response to standard treatments, with median survival under 15 months. The SIX transcription factor family has been implicated in tumor development, but the role and regulatory mechanism of SIX5 in glioblastoma (GBM) remain unclear. This study systematically investigates the biological function of SIX5 and its regulatory network in GBM. Differential expression and weighted gene co-expression network analyses of GSE4290 and GSE50161 datasets, combined with machine learning algorithms including LASSO, identified SIX5 as a core candidate gene. Functional enrichment analyses and evaluation using TCGA and UALCAN databases revealed that SIX5 is highly expressed in GBM and associated with poor prognosis. Single-cell RNA sequencing and spatial transcriptomics showed enrichment of SIX5 in the tumor core and in astrocyte-like and stem cell-like subsets at the invasion front.
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