Han, Myung Woul Lee, Jong Cheol Choi, Jun-Young Kim, Gui Chul Chang, Hyo Won Nam, Hae Yun Kim, Seong Who Kim, Sang Yoon 2024-01-20T10:04:50Z 2024-01-20T10:04:50Z 2021-09-05 2014-03 0250-7005 https://pubs.kist.re.kr/handle/201004/127033 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. English INT INST ANTICANCER RESEARCH MALIGNANT GLIOMA-CELLS APOPTOSIS RADIATION TARGET MACROAUTOPHAGY CHEMOTHERAPY THERAPY Autophagy Inhibition Can Overcome Radioresistance in Breast Cancer Cells Through Suppression of TAK1 Activation Article 1 ANTICANCER RESEARCH, v.34, no.3, pp.1449 - 1455 ANTICANCER RESEARCH 34 3 1449 1455 scie scopus 000333377800049 2-s2.0-84898912571 Oncology Oncology Article MALIGNANT GLIOMA-CELLS APOPTOSIS RADIATION TARGET MACROAUTOPHAGY CHEMOTHERAPY THERAPY Autophagy radioresistance TAK1 breast cancer