AI Article Synopsis
- Autophagy is often activated in cancer cells that resist radiation, prompting researchers to study its relationship with TAK1 in this context.
- The study found that inhibiting TAK1 increased the effectiveness of radiation treatment in MDA-MB231 breast cancer cells by promoting cell death.
- Overall, the results suggest that targeting TAK1 and autophagy could be a promising approach for improving treatment outcomes in radioresistant breast cancer.
Article Abstract
Background/aim: Autophagy is frequently activated in radioresistant cancer cells. In the present study, we evaluated the role of autophagy and transforming growth factor-activated kinase 1 (TAK1) in radioresistance.
Materials And Methods: TAK1 phosphorylation in MDA-MB231 breast cancer cells was evaluated by western blotting. The regulatory effects of the TAK1 inhibitor and autophagy inhibitor were assessed by cell morphology, cell survival and induction of apoptosis.
Results: Radiation induced the phosphorylation of TAK1, whereas the inhibition of TAK1 activity enhanced the cytotoxicity of radiation in MDA-MB231 cells. Autophagy inhibitors significantly enhanced radiation-induced apoptosis of MDA-MB231 cells. This augmentation in radiosensitivity seemed to result from the suppression of TAK1 activation.
Conclusion: Inhibition of autophagy enhanced radiosensitivity through suppression of radiation-induced TAK1 activation, suggesting that the modulation of TAK1-induced autophagy may be a good therapeutic strategy to treat radioresistant breast cancer.
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