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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Wang, Z. Zeng, Q. Chen, T. Liao, K. Bu, Y. Hong, S. Hu, G. |
| Description | Country affiliation: China Author Affiliation: Wang Z ( Department of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.); Zeng Q ( Department of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.); Chen T ( Department of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.); Liao K ( Department of Oncology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.); Bu Y ( Department of Biochemistry and Molecular Biology, Molecular Medicine and Cancer Research, China Center, Chongqing Medical University, Chongqing, China.); Hong S ( Department of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.); Hu G ( Department of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.) |
| Abstract | NFBD1 functions in cell cycle checkpoint activation and DNA repair following ionizing radiation (IR). In this study, we defined the NFBD1 as a tractable molecular target to radiosensitize nasopharyngeal carcinoma (NPC) cells. Silencing NFBD1 using lentivirus-mediated shRNA-sensitized NPC cells to radiation in a dose-dependent manner, increasing apoptotic cell death, decreasing clonogenic survival and delaying DNA damage repair. Furthermore, downregulation of NFBD1 inhibited the amplification of the IR-induced DNA damage signal, and failed to accumulate and retain DNA damage-response proteins at the DNA damage sites, which leaded to defective checkpoint activation following DNA damage. We also implicated the involvement of NFBD1 in IR-induced Rad51 and DNA-dependent protein kinase catalytic subunit foci formation. Xenografts models in nude mice showed that silencing NFBD1 significantly enhanced the antitumor activity of IR, leading to tumor growth inhibition of the combination therapy. Our studies suggested that a combination of gene therapy and radiation therapy may be an effective strategy for human NPC treatment. |
| File Format | HTM / HTML |
| e-ISSN | 20414889 |
| DOI | 10.1038/cddis.2015.214 |
| Journal | Cell Death and Disease |
| Volume Number | 6 |
| Language | English |
| Publisher | Nature Publishing Group |
| Publisher Date | 2015-08-06 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Therapy Gamma Rays Research Support, Non-u.s. Gov't Dna Repair Intracellular Signaling Peptides And Proteins Radiation Tolerance Gene Expression Regulation, Neoplastic Dna Damage Antagonists & Inhibitors Genetics Nasopharyngeal Neoplasms Rad51 Recombinase Signal Transduction Rna, Small Interfering Tumor Burden Metabolism Xenograft Model Antitumor Assays Discipline Cell Biology Pathology Animals Mice, Nude Radiation Effects Mice Hela Cells Apoptosis |
| Content Type | Text |
| Resource Type | Article |
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