Abstract
Many human tumor cells are characterized by overexpression or mutation of epidermal growth factor receptor (EGFR). Emerging evidence indicates that EGFR, as well as some of its downstream components, can translocate to the nucleus and play roles in transcriptional regulation, signaling conduction and repair of DNA double strands breaks (DSBs). EGFR in its nuclear manifestation promotes DSB repair by interacting with proteins including DNA-PK, ATM, Rad51 and BRCA1, involved in DSB repair, via the PI3K-Akt and Ras-Raf-MAPK pathways. DNA damage repair in tumor cells is emerging as an attractive target in radiotherapy and chemotherapy. Interruption of EGFR functions, or those of its downstream components, presents a promising strategy for confounding DNA damage repair in tumor cells.
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Lu, J., Yang, L., Tao, Y. et al. Role of epidermal growth factor receptor in DNA damage repair. Chin. Sci. Bull. 56, 3132–3137 (2011). https://doi.org/10.1007/s11434-011-4650-5
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DOI: https://doi.org/10.1007/s11434-011-4650-5