Silencing of TGase 2 sensitizes breast cancer cells to apoptosis by regulation of survival factors

Dae Seok Kim, Kang Seo Park, Soo Youl Kim

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

The cross-linking enzyme, Transglutaminase 2 (TGase 2), contributes to physiological homeostasis and plays a role in cell death and survival. We previously showed that down-regulation of TGase 2 by cystamine or synthetic peptide R2 promotes apoptosis in drug-resistant cancer cells by restoring the level of I-κBα, leading to inactivation of NF-κB. To better define the action of TGase 2, its expression was blocked by small interfering RNA. This interference rendered, the doxorubicin-resistant breast cancer cells, highly susceptible to doxorubicin-induced apoptosis. This susceptibility, was associated with decreased levels of the cell-survival factors BCl2 and BCLXL whereas the level of BAX remained un-changed. Together, the findings support the view that TGase 2 leads to drug-resistance by up-regulating the level of survival factors via NF-κB activation.

Original languageEnglish (US)
Pages (from-to)2514-2521
Number of pages8
JournalFrontiers in Bioscience
Volume14
Issue number7
DOIs
StatePublished - Jan 1 2009
Externally publishedYes

Keywords

  • BCl
  • I-κBα
  • NF-κB
  • siRNA
  • TGase 2

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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