Radioresistance of cancer cells, integrin αvβ3 and thyroid hormone
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John T. Leith1, Shaker A. Mousa2, Aleck Hercbergs3, Hung-Yun Lin4,5,6,7 and Paul J. Davis2,8
1Rhode Island Nuclear Science Center, Narragansett, RI, USA
2Pharmaceutical Research Institute, Albany College of Pharmacy and Health Sciences, Rensselaer, NY, USA
3Department of Radiation Oncology, Cleveland Clinic, Cleveland, OH, USA
4Taipei Cancer Center, Taipei Medical University, Taipei, Taiwan
5PhD Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan
6Traditional Herbal Medicine Research Center, Taipei Medical University, Taipei, Taiwan
7TMU Research Center of Cancer Translational Medicine, Taipei Medical University, Taipei, Taiwan
8Department of Medicine, Albany Medical College, Albany, NY, USA
Paul J. Davis, email: [email protected]
Keywords: integrin open configuration; AKT; epithelial-mesenchymal transition (EMT); L-thyroxine (T4); STAT3
Received: August 30, 2018 Accepted: November 16, 2018 Published: December 11, 2018
Radioresistance is a substantial barrier to success in cancer management. A number of molecular mechanisms support radioresistance. We have shown experimentally that the thyroid hormone analogue receptor on the extracellular domain of integrin αvβ3 may modulate the state of radiosensitivity of tumor cells. Specifically, tetraiodothyroacetic acid (tetrac), a derivative of L-thyroxine (T4), can reduce radioresistance in cancer cells. In this review, we list a number of intrinsic signal transduction molecules and other host factors that have been reported to support/induce radioresistance in cancer cells and that are also subject to control by T4 through actions primarily initiated at integrin αvβ3. Additional preclinical evidence is needed to support these radioresistance-relevant actions of thyroid hormone.
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