Journal
HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK
Volume 38, Issue -, Pages E1909-E1917Publisher
WILEY
DOI: 10.1002/hed.24347
Keywords
beta-catenin; LKB1/AMP-activated protein kinase (LKB1/AMPK); Ku70/Ku80; radiation sensitivity; head and neck cancer cells
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Funding
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science, ICT, and Future planning [NRF-2014R1A1A1003484, NRF-2015R1A2A1A01003050]
- Korean Health Technology R&D Project, Ministry of Health & Welfare of the Republic of Korea [A120216]
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Background. We attempted to elucidate the mechanism of cell death after radiation by studying how beta-catenin silencing controls the radiation sensitivity of radioresistant head and neck cancer cells. Methods. The most radioresistant cancer cell line (AMC-HN-9) was selected for study. Targeted silencing of beta-catenin was used on siRNAs. Sensitivity to radiation was examined using clonogenic and methylthiazol tetrazolium (MTT) assays. Results. A combination of irradiation plus beta-catenin silencing led to a significant reduction in the inherent radioresistance of AMC-HN-9 cells. Although expression of Ku70/80 was upregulated in AMC-HN-9 cells after irradiation, Ku70/80 was dramatically decreased in a combination of irradiation and beta-catenin silencing. Interestingly, irradiation-induced Ku70/80 was completely prevented by beta-catenin silencing-induced LKB1/AMP-activated protein kinase (LKB1/AMPK) signal. Conclusion. The LKB1/AMPK pathway might relay the signal between the Wnt/beta-catenin pathway and the Ku70/Ku80 DNA repair machinery, and play a decisive role in fine-tuning the responses of cancer cells to irradiation. (C) 2015 Wiley Periodicals, Inc.
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