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EGFR inhibitor C225 increases the radiosensitivity of human lung squamous cancer cells
BACKGROUND: The purpose of the present study is to investigate the direct biological effects of the epidermal growth factor receptor (EGFR) inhibitor C225 on the radiosensitivity of human lung squamous cancer cell-H520. H520 cells were treated with different dosage of (60)Co γ ray irradiation (1.953...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2972262/ https://www.ncbi.nlm.nih.gov/pubmed/20969791 http://dx.doi.org/10.1186/1475-2867-10-39 |
Sumario: | BACKGROUND: The purpose of the present study is to investigate the direct biological effects of the epidermal growth factor receptor (EGFR) inhibitor C225 on the radiosensitivity of human lung squamous cancer cell-H520. H520 cells were treated with different dosage of (60)Co γ ray irradiation (1.953 Gy/min) in the presence or absence of C225. The cellular proliferation, colony forming capacity, apoptosis, the cell cycle distribution as well as caspase-3 were analyzed in vitro. RESULTS: We found that C225 treatment significantly increased radiosensitivity of H-520 cells to irradiation, and led to cell cycle arrest in G(1 )phase, whereas (60)Co γ ray irradiation mainly caused G(2 )phase arrest. H-520 cells thus displayed both the G(1 )and G(2 )phase arrest upon treatment with C225 in combination with (60)Co γ ray irradiation. Moreover, C225 treatment significantly increased the apoptosis percentage of H-520 cells (13.91% ± 1.88%) compared with the control group (5.75% ± 0.64%, P < 0.05). CONCLUSION: In this regard, C225 treatment may make H-520 cells more sensitive to irradiation through the enhancement of caspase-3 mediated tumor cell apoptosis and cell cycle arrest. |
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