Host: The Japan Radiation Research Society
It is supposed that p53 gene function, as a gene guardian, controls cell cycle proceeding or induction of apoptosis, and suppresses the process of malignant transformation when DNA is damaged. However, we don't know exactly whether p53 gene function relates to malignant transformation or not. We studied to be clear whether p53 function related to cell immortalization or malignant transformation.In our study, we established four cell lines from C57BL embryo mouse, which included two normal p53 gene function cell lines (p53+/+) and two p53 gene knock-out cell lines (p53-/-). By the normal cell culture way, all of cells acquired the immortalization whether p53 function was positive or negative and whether the cells were irradiated or not. If p53, which responses to DNA damage stress, relates to cell malignant transformation, we expected that cell malignant transformation of p53-/- cells promote by X-ray irradiation. So we studied the frequency of the chromosome aberration in X-ray irradiated cells. As a result, p53+/+ cells became tetraploid cells both with or without irradiation. At 40-41 passages, 30-60% of p53+/+ cells became tetraploid cells. On the other hand, p53-/- cells became triploid (40-50%) rather than tetraploid both with or without X-rradiation. We observed that non-irradiated p53-/- cells, at passage 38 or 90, initiated tumors upon transplantation of the cells under back skin of nude mouse, but non-irradiated p53+/+ cells did not. Interestingly, both the cells before transplantation and the tumor cells were triploid cells mainly. This suggested that triploidy was related to cell malignant transformation closely.