Open Access
Article
Silencing of TGase 2 sensitizes breast cancer cells to apoptosis by regulation of survival factors
Dae-Seok Kim1,Kang-Seo Park1,Soo-Youl Kim1
1
Molecular Oncology Branch, Division of Basic and Applied Science, Research Institute, National Cancer Center, Goyang, Kyonggi-do, Republic of Korea
DOI: 10.2741/3394 Volume 14 Issue 7, pp.2514-2521
Published: 01 January 2009
(This article belongs to the Special Issue Cellular functions of tissue transglutaminase)
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-kBa, leading to inactivation of NF-kB. 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-kB activation.

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Dae-Seok Kim, Kang-Seo Park, Soo-Youl Kim. Silencing of TGase 2 sensitizes breast cancer cells to apoptosis by regulation of survival factors. Frontiers in Bioscience-Landmark. 2009. 14(7); 2514-2521.