1. Tob1 enhances radiosensitivity of breast cancer cells involving the JNK and p38 pathways.
- Author
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Wu D, Zhou W, Wang S, Zhou Z, Wang S, and Chen L
- Subjects
- Cell Line, Tumor, Cell Survival physiology, Cell Survival radiation effects, Female, Humans, Intracellular Signaling Peptides and Proteins radiation effects, MAP Kinase Signaling System radiation effects, Tumor Suppressor Proteins radiation effects, p38 Mitogen-Activated Protein Kinases radiation effects, Breast Neoplasms metabolism, Intracellular Signaling Peptides and Proteins biosynthesis, MAP Kinase Signaling System physiology, Radiation Tolerance physiology, Tumor Suppressor Proteins biosynthesis, p38 Mitogen-Activated Protein Kinases biosynthesis
- Abstract
The aim of the present study was to evaluate the effect of Tob1 on the radiosensitivity of breast cancer cells. The results showed that overexpression of Tob1 reduced the clonogenic growth of 231 cells and induced the rate of apoptosis. Tob1 caused an accumulation of cells in the G0 /G1 phase and decreased the percentage of cells in S phase. We also found that overexpression of Tob1 significantly reduced the phosphorylation of JNK and p38. The activator of JNK and p38, anisomycin, attenuated the blockage of Tob1 on the cell cycle and reversed the effect of Tob1 on apoptosis. Taken together, Tob1 enhanced radiosensitivity of breast cancer cells through regulation of the JNK and p38 pathways. The results indicated that Tob1 might be a promising molecular in gene therapy for the treatment of breast cancer., (© 2015 International Federation for Cell Biology.)
- Published
- 2015
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