Radiosensitization of HNSCC cells by EGFR inhibition depends on the induction of cell cycle arrests.

摘要: The increase in cellular radiosensitivity by EGF receptor (EGFR) inhibition has been shown to be attributable the induction of a G1-arrest p53-proficient cells. Because EGFR targeting combination with radiotherapy is used treat head and neck squamous cell carcinomas (HNSCC) which are predominantly p53 mutated, we tested effects on radiosensitivity, proliferation, apoptosis, DNA repair cycle control using large panel HNSCC lines. In these experiments inhibited signal transduction, blocked proliferation induced radiosensitization but only some lines under normal (pre-plating) conditions. This sensitization was not associated impaired (53BP1 foci) or apoptosis. However, it lasting G2-arrest. Both, G2-arrest were abrogated if cells re-stimulated (delayed plating) actually no being detectable any 14 Therefore conclude that can induce reversible G2 arrest deficient cells, does consequently result robust radiosensitization. Together recent animal clinical studies our data indicate effective strategy