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Your search keyword '"Chang, Hyo Won"' showing total 3 results
Start Over Author "Chang, Hyo Won" Journal anticancer research
3 results on '"Chang, Hyo Won"'

1. Periostin Plays a Key Role in Radioresistance of Head and Neck Cancer Cells Via Epithelial-to-Mesenchymal Transition

Author

PARK, JUNG JE, primary, HAH, YOUNG-SOOL, additional, RYU, SOMI, additional, CHEON, SO YOUNG, additional, CHO, HEE YOUNG, additional, KIM, JIN PYEONG, additional, WON, SEONG JUN, additional, LEE, JONG SIL, additional, HWA, JEONG SEOK, additional, SEO, JI HYUN, additional, CHANG, HYO WON, additional, and KIM, SANG YOON, additional

Published
2020
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3. Autophagy inhibition can overcome radioresistance in breast cancer cells through suppression of TAK1 activation.

Author

Han MW, Lee JC, Choi JY, Kim GC, Chang HW, Nam HY, Kim SW, and Kim SY

Subjects
Antifungal Agents pharmacology, Antimalarials pharmacology, Autophagy radiation effects, Blotting, Western, Breast Neoplasms drug therapy, Breast Neoplasms radiotherapy, Cell Proliferation drug effects, Cell Proliferation radiation effects, Chloroquine pharmacology, Female, Gamma Rays, Gene Expression Regulation, Neoplastic radiation effects, Humans, Macrolides pharmacology, Phosphorylation drug effects, Signal Transduction radiation effects, Tumor Cells, Cultured, Autophagy drug effects, Breast Neoplasms metabolism, Breast Neoplasms pathology, Gene Expression Regulation, Neoplastic drug effects, MAP Kinase Kinase Kinases metabolism, Radiation Tolerance drug effects, Signal Transduction drug effects
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.

Published
2014

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