| Objective:Since the extensive application of nuclear energy and the development of nuclear technology, the carcinogenesis risks of low dose radiation (LDR) (<100 mGy) has become much attractive, but its molecular mechanism remains elusive. Applied human bronchial epithelial cells, this thesis studied the potential possibilities and underlying mechanisms of long-term LDR induced malignant transformation.Methods:Human immortalized bronchial epithelial cells Beas-2B were irradiated with 0.025 Gy a-particles every 4 days for 8 times in total and then further cultured for 1-2 months. Cell proliferation, adhesion, invasion, and the levels of malignant transformation related proteins were measured. siRNA transfection was used to test the role of p38 in the above changes.Results:Cell proliferation and the abilities of adhesion and invasion were obviously increased after multiple LDR of a-particles. These increments could be maintained in the offspring of irradiated cells for 1-2 months after the final exposure, and the cell invasive ability was even high in the daughter cells after 2 months of LDR, indicating a potential of cell malignant transformation. Further measurements showed that the protein expressions of p-Akt, p-P38 and p-ERK were significantly increased in the irradiated cells as well as its progeny after 2 months of irradiation. In addition, p-JNK was over-expressed in the irradiated cells but it had a lower level in the subcultures 1-2 months after irradiation, but the protein levels of p-P66 in the irradiated cells and its offspring were only about half of the non-irradiated control. Moreover, when the cells were transferred with p38 siRNA, LDR-induced enhancements of cell adhesion and invasion were significantly diminished.Conclusions:Long-term LDR of a-particles could enhance the potential of malignant transformation incidence in human bronchial epithelial cells through MAPK/Akt pathway. |
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