ArticleCNS neuroscience & therapeutics2026
Tumor Electric Field Therapy Inhibits Epithelial-Mesenchymal Transition, Invasion, and Migration of Glioblastoma by Targeting the c-FOS/CXCL14 Axis.
Article in CNS neuroscience & therapeutics, 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
backgroundGlioblastoma (GBM) is among the most aggressive and treatment-resistant primary brain tumors. The mesenchymal subtype of GBM shows a particularly unfavorable prognosis. Epithelial-mesenchymal transition (EMT) is a critical phenotypic characteristic of this subtype. Tumor electric field therapy (TEFT) has emerged as a promising adjuvant therapy, but its underlying anti-GBM mechanisms remain incompletely elucidated.
methodsKey molecular targets of TEFT were identified through integrated multi-omics data analysis. U87, U251, and T98G cell lines received TEFT treatment at 200 kHz and 2.2 V/cm for 72 h. Stable cell models with CXCL14 and c-FOS knockdown or overexpression were established using lentiviral vectors. Cellular phenotypes were assessed via wound healing assays, transwell migration and invasion assays, and western blot analysis. The regulatory hierarchy between c-FOS and CXCL14 was verified via chromatin immunoprecipitation (ChIP) assays and rescue experiments. Mechanistic insights were validated in orthotopic nude mouse models and clinical patient specimens.
resultsCXCL14 was identified by integrated bioinformatics analysis. It showed significant overexpression in mesenchymal subtypes and was strongly associated with poor prognosis. Single-cell sequencing analysis suggested a significant increase in the EMT score of the subgroup with high CXCL14 expression. TEFT induced a morphological shift from mesenchymal to epithelial-like characteristics. It downregulated mesenchymal markers, including N-cadherin, Vimentin, and Snail, while upregulating E-cadherin. Mechanistic investigations demonstrated that TEFT promoted the degradation of c-FOS, leading to CXCL14 downregulation and subsequent inhibition of EMT. In vivo experiments confirmed the critical role of the c-FOS/CXCL14 axis in regulating GBM invasion and migration potential.
conclusionThis study first revealed a novel mechanism which TEFT suppressed EMT in GBM via the c-FOS/CXCL14 axis. These findings provided a new therapeutic target and a theoretical foundation for optimizing TEFT efficacy.
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