The DOI matches its Crossref record; 449 of the 449 references it cites were found in a registry or an index.
DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer
Open accessAbstract
Radiotherapy is one of the most common countermeasures for treating a wide range of tumors. However, the radioresistance of cancer cells is still a major limitation for radiotherapy applications. Efforts are continuously ongoing to explore sensitizing targets and develop radiosensitizers for improving the outcomes of radiotherapy. DNA double-strand breaks are the most lethal lesions induced by ionizing radiation and can trigger a series of cellular DNA damage responses (DDRs), including those helping cells recover from radiation injuries, such as the activation of DNA damage sensing and early transduction pathways, cell cycle arrest, and DNA repair. Obviously, these protective DDRs confer tumor radioresistance. Targeting DDR signaling pathways has become an attractive strategy for overcoming tumor radioresistance, and some important advances and breakthroughs have already been achieved in recent years. On the basis of comprehensively reviewing the DDR signal pathways, we provide an update on the novel and promising druggable targets emerging from DDR pathways that can be exploited for radiosensitization. We further discuss recent advances identified from preclinical studies, current clinical trials, and clinical application of chemical inhibitors targeting key DDR proteins, including DNA-PKcs (DNA-dependent protein kinase, catalytic subunit), ATM/ATR (ataxia–telangiectasia mutated and Rad3-related), the MRN (MRE11-RAD50-NBS1) complex, the PARP (poly[ADP-ribose] polymerase) family, MDC1, Wee1, LIG4 (ligase IV), CDK1, BRCA1 (BRCA1 C terminal), CHK1, and HIF-1 (hypoxia-inducible factor-1). Challenges for ionizing radiation-induced signal transduction and targeted therapy are also discussed based on recent achievements in the biological field of radiotherapy.
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2 retracted
BRCA1 Phosphorylation by Aurora-A in the Regulation of G2 to M Transition
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Cited by
Juan, C. A., Pérez de la Lastra, J. M., Plou, F. J., & Pérez-Lebeña, E. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22094642 · Cited by 2,810
Matthews, H. K., Bertoli, C., & de Bruin, R. A. M. (2022) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-021-00404-3 · Cited by 1,506
Huang, R., & Zhou, P.-K. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00648-7 · Cited by 907
Self-citationHu, D., Li, Y., Li, R., Wang, M., Zhou, K., He, C., Wei, Q., & Qian, Z. (2024) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2024.10.015 · Cited by 153
Fighting Drug Resistance through the Targeting of Drug-Tolerant Persister Cells
De Conti, G., Dias, M. H., & Bernards, R. (2021) · Cancers · doi:10.3390/cancers13051118 · Cited by 111
Metadata
- Authors
- Huang, R.-X., & Zhou, P.-K.
- Venue
- Signal Transduction and Targeted Therapy
- Published
- 2020-05-01
- Volume
- 5
- Issue
- 1
- Pages
- 60-60
- ISSN
- 2059-3635 (ISSN-L)
- OpenAlex
- W3022486080
- Cited by
- 1,198
- References
- 449
- FWCI
- 33.75
- Type
- journal article
- Language
- en
- Open access
- gold
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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