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Updated: Feb 4, 2026

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
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Transglutaminase 2 exacerbates ovarian cancer survival by directly inactivating GSK3β

Ho Lee1,2, Joon Hee Kang1,2, Hyun Jung Kim3

  • 1Division of Cancer Biology, National Cancer Center, Goyang, Gyeonggi, Republic of Korea.

Cell Death & Disease
|February 2, 2026
PubMed

Insights

Transglutaminase 2 (TGase 2) drives ovarian cancer metastasis and drug resistance by promoting epithelial-mesenchymal transition (EMT). Inhibiting TGase 2 interaction with GSK3β offers a novel therapeutic strategy to overcome treatment challenges.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ovarian cancer frequently recurs with metastasis despite initial chemotherapy response.
  • Drug-resistant ovarian cancer cells show elevated transglutaminase 2 (TGase 2) levels, linked to epithelial-mesenchymal transition (EMT) and chemotherapy evasion.
  • TGase 2 is crucial for maintaining the mesenchymal phenotype, but its mechanism in promoting EMT is unclear.

Purpose of the Study:

  • To elucidate the mechanism by which TGase 2 promotes EMT in ovarian cancer.
  • To identify TGase 2 as a therapeutic target for overcoming drug resistance and metastasis.

Main Methods:

  • Investigated the interaction between TGase 2 and glycogen synthase kinase-3β (GSK3β).
  • Utilized domain mapping to identify the interaction site between TGase 2 and GSK3β.
  • Assessed the effect of pharmacological inhibition of the TGase 2-GSK3β interaction in a xenograft model.

Main Results:

  • TGase 2 directly binds to GSK3β, promoting β-catenin stabilization and EMT.
  • The N-terminus of TGase 2 interacts with the mid-region of GSK3β, leading to GSK3β autophagic degradation.
  • Pharmacological disruption of this interaction with streptonigrin, combined with chemotherapy, improved survival in ovarian cancer xenografts.

Conclusions:

  • TGase 2 is a key regulator of EMT, metastasis, and drug resistance in ovarian cancer.
  • Targeting the TGase 2-GSK3β interaction presents a promising therapeutic strategy for advanced ovarian cancer.

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