Related Experiment Video
Updated: Jan 4, 2026
Trans-vivo Delayed Type Hypersensitivity Assay for Antigen Specific Regulation
Published on: May 2, 2013
Effect of Tissue Transglutaminase on Steroid Resistance in T-Cell Acute Lymphoblastic Leukemia
Hyun Joo Jung1, Eun Hee Han1, In Keun Jang2
1Department of Pediatrics, Ajou University Hospital, Ajou University School of Medicine, Suwon, Republic of Korea.
Aim:
To improve survival in patients with glucocorticoid-resistant T-cell acute lymphoblastic leukemia (T-ALL), it is critical to develop new therapeutic strategies to overcome steroid resistance.
Materials And Methods:
Biochemical and molecular methodologies were used to evaluate whether tissue transglutaminase (TG2) confers steroid resistance in T-ALL.
Results:
T-ALL cells were found to express elevated levels of TG2. Models of steroid-adapted subclones of T-ALL cell lines which were notably less sensitive to steroids than the parental cells. The steroid-adapted subclones showed increased TG2 expression and nuclear factor-κB (NF-κB) activity compared to T-ALL parental cells. Inhibition of TG2 suppressed steroid resistance and improved steroid cytotoxicity in steroid-adapted subclones of T-ALL in association with reduced NF-κB activity.
Conclusion:
TG2 may serve as a new target to overcome steroid resistance in T-ALL.
Insights
Tissue transglutaminase (TG2) may overcome steroid resistance in T-cell acute lymphoblastic leukemia (T-ALL). Inhibiting TG2 suppressed steroid resistance and improved treatment effectiveness in T-ALL cells.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glucocorticoid resistance in T-cell acute lymphoblastic leukemia (T-ALL) poses a significant challenge to patient survival.
- Novel therapeutic strategies are essential to overcome steroid resistance in T-ALL.
Purpose of the Study:
- To investigate the role of tissue transglutaminase (TG2) in conferring steroid resistance in T-ALL.
- To evaluate TG2 as a potential therapeutic target for glucocorticoid-resistant T-ALL.
Main Methods:
- Utilized biochemical and molecular methodologies to assess TG2 expression and activity.
- Developed and analyzed steroid-adapted T-ALL cell line subclones to model resistance.
- Measured nuclear factor-κB (NF-κB) activity in relation to TG2 and steroid sensitivity.
Main Results:
- T-ALL cells exhibited elevated TG2 levels.
- Steroid-adapted subclones showed decreased steroid sensitivity, increased TG2 expression, and heightened NF-κB activity.
- TG2 inhibition effectively suppressed steroid resistance and enhanced steroid cytotoxicity, correlating with reduced NF-κB activity.
Conclusions:
- Tissue transglutaminase (TG2) is implicated in the development of steroid resistance in T-ALL.
- Targeting TG2 presents a promising strategy to overcome glucocorticoid resistance in T-ALL patients.
