ArticleFrontiers in immunology2025
Administration of 2-deoxy-D-glucose induces pyroptosis in murine breast cancer cells via cAMP/PKA/HK2 to impair tumor survival.
Article in Frontiers in immunology, 2025. 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
Background: Breast cancer poses a severe threat owing to its high morbidity and mortality rates, which are largely attributed to drug resistance. Therefore, novel therapeutic targets need to be identified. Pyroptosis is an inflammatory cell death process mediated by gasdermin (GSDM) and dependent on caspases. Moreover, pyroptosis plays a role in regulating tumor progression and response to therapy. Furthermore, 2-deoxy-D-glucose (2-DG) is a glucose analogue that confers anticancer effects via metabolic interference. However, its mechanism of action in breast cancer remains unclear. Methods: To explore the effect of 2-DG on pyroptosis in EMT6/4T1 breast cancer cells, cell viability assays, immunoblotting, immunofluorescence, co-immunoprecipitation, and morphological analyses were performed. For Results: 2-DG induced cytotoxicity and pyroptosis in EMT6/4T1 breast cancer cells. Mechanistically, 2-DG activated cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signalling, suppressed hexokinase 2 (HK2), and triggered caspase-3/GSDME-dependent pyroptosis. Conclusions: These findings identified a novel metabolic-inflammatory axis (cAMP/PKA-HK2-caspase-3/GSDME) in breast cancer. Furthermore, study highlights the
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