ArticleCell death & disease2026
Transglutaminase 2 exacerbates ovarian cancer survival by directly inactivating GSK3β.
Article in Cell death & disease, 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
Elevated expression of transglutaminase 2 (TGase 2, EC 2.3.2.13, protein-glutamine γ-glutamyltransferase, gene name TGM2) is known as one of the most upregulated genes during epithelial-mesenchymal transition (EMT) in ovarian cancer. Despite initial complete responses to conventional chemotherapy, ovarian cancer often recurs with metastasis, presenting a significant clinical challenge. Drug-resistant ovarian cancer cells exhibit markedly higher levels of TGase 2 compared to normal ovarian epithelium, which is associated with EMT activation, enabling them to evade chemotherapy effects. Intracellular TGase 2 is recognized as a key factor in maintaining the mesenchymal phenotype. Therefore, while EMT expression can be effectively reversed by inhibiting TGase 2, the underlying mechanism of this effect remains unclear. We found that TGase 2 promotes EMT by directly binding to glycogen synthase kinase-3β (GSK3β), promoting the stabilization of β-catenin. Domain mapping revealed that the N-terminus of TGase 2 interacts with the mid-region of GSK3β, leading to the autophagic degradation of GSK3β. Pharmacological disruption of this N-terminal interaction by streptonigrin, in combination with standard chemotherapy, extended overall survival in a xenograft model of ovarian cancer. This study identified TGase 2 as a pivotal regulator of EMT-driven metastasis and drug resistance.
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