@article{0afc2687161f4f3f8b8161f1ecb3dfb7,
title = "Cellular processing determinants for the activation of damage signals in response to topoisomerase I-linked DNA breakage",
abstract = "Recent studies have suggested an involvement of processing pathways for the initiation of cellular responses induced by topoisomerase-targeting drugs. Here, we showed that cellular exposure to camptothecin (CPT) induced formation of topoisomerase I cleavable complex (TOP1cc), degradation of TOP1 and activation of DNA damage responses (DDR). Transcription and proteasome-dependent proteolysis, but not replication, were involved in CPT-induced TOP1 degradation, while none of above three processing activities affected TOP1cc formation. Replication-and transcription-initiated processing (RIP and TIP) of TOP1cc were identified as two independent pathways, which contribute distinctly to various CPT-activated DDR. Specifically, in cycling cells, RIP-processed TOP1cc triggered the CPT-induced RPA phosphorylation. At higher CPT dosages, the TIP pathway is required for other DDR activation, including ATM, p53 and Chk1/2 phosphorylation. The TIP pathway was further demonstrated to be S-phase independent by using three nonreplicating cell models. Furthermore, the effect of proteasome inhibitors mimicked that of transcription inhibition on the CPT-induced activation of DDR, suggesting the involvement of proteasome in the TIP pathway. Interestingly, the TIP pathway was important for TOP1cc-activated, but not ionization radiation-activated ATM, p53 and Chk2 phosphorylation. We have also found that pharmacological interferences of TIP and RIP pathways distinctively modulated the CPT-induced cell killing with treatments at low and high dosages, respectively. Together, our results support that both RIP and TIP pathways of TOP1cc are required for the activation of CPT-induced DDR and cytotoxicity. {\textcopyright} 2010 IBCB, SIBS, CAS. All rights reserved.",
keywords = "cleavable complex, DNA damage responses, downregulation, processing, protein-linked DNA break, ATM protein, camptothecin, cell cycle protein, checkpoint kinase 2, DNA binding protein, DNA topoisomerase, protein p53, protein serine threonine kinase, replication factor A, RPA2 protein, human, tumor suppressor protein, article, DNA repair, DNA replication, DNA strand breakage, genetic transcription, genetics, human, metabolism, phosphorylation, signal transduction, tumor cell line, Camptothecin, Cell Cycle Proteins, Cell Line, Tumor, DNA Breaks, DNA Repair, DNA Replication, DNA Topoisomerases, Type I, DNA-Binding Proteins, Humans, Phosphorylation, Protein-Serine-Threonine Kinases, Replication Protein A, Signal Transduction, Transcription, Genetic, Tumor Suppressor Protein p53, Tumor Suppressor Proteins",
author = "Ting-Hsiang Huang and Hsiang-Chin Chen and Shang-Min Chou and Yu-Chen Yang and Jia-Rong Fan and Tsai-Kun Li",
note = "被引用次數:8 Export Date: 7 April 2016 通訊地址: Li, T.-K.; Department and Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Jen-Ai Road, Taipei 10018, Taiwan; 電子郵件: tsaikunli@ntu.edu.tw 化學物質/CAS: DNA topoisomerase, 80449-01-0; camptothecin, 7689-03-4; checkpoint kinase 2, 244634-79-5; Camptothecin, 7689-03-4; Cell Cycle Proteins; DNA Topoisomerases, Type I, 5.99.1.2; DNA-Binding Proteins; Protein-Serine-Threonine Kinases, 2.7.11.1; RPA2 protein, human, 2.7.7.7; Replication Protein A; Tumor Suppressor Protein p53; Tumor Suppressor Proteins; ataxia telangiectasia mutated protein, 2.7.1.37; checkpoint kinase 2, 2.7.1.37 參考文獻: Zhou, B.B., Bartek, J., Targeting the checkpoint kinases: Chemo-sensitization versus chemoprotection (2004) Nat Rev Cancer, 4, pp. 216-225; Falck, J., Coates, J., Jackson, S.P., Conserved modes of recruitment of ATM. 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year = "2010",
doi = "10.1038/cr.2010.95",
language = "English",
volume = "20",
pages = "1060--1075",
journal = "Cell Research",
issn = "1001-0602",
publisher = "Nature Publishing Group",
number = "9",
}