ArticleNature communications2026
α-KG conformationally stabilizes nuclear GLUD1-SNAIL complex to fuel trans-endothelial migration in metastasis.
Article in Nature communications, 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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15 authors.
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Abstract
Trans-endothelial migration (TEM) is a critical rate-limiting barrier in tumor metastasis, yet its mechanistic basis remains poorly defined. Here we show that α-ketoglutarate (α-KG) and its metabolic enzyme glutamate dehydrogenase 1 (GLUD1) constitute a pivotal regulatory axis governing this process. Mechanistically, GLUD1 translocates to the nucleus, where α-KG binds to its non-catalytic site (K147) to induce a conformational change that stabilizes the GLUD1-SNAIL interaction, promoting assembly of a nuclear ternary complex. Notably, this complex is preferentially enriched in tumors, and specific blockade of K147 disrupts this assembly and abrogates metastatic effects. Our findings reveal a non-canonical role for GLUD1 and α-KG in transcriptional regulation and propose a therapeutic paradigm that selectively interferes with metabolite-dependent complex formation rather than enzymatic activity, offering a precise strategy to target TEM-driven metastatic cells.
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