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机构地区:[1]北京医科大学生物化学与分子生物学系,100083
出 处:《北京医科大学学报》1997年第1期18-20,共3页Journal of Peking University(Health Sciences)
摘 要:目的:观察野生型p53对胃癌细胞系的生长抑制作用。方法:以逆转录病毒为载体将野生型p53基因导入胃癌细胞系MKN28和BGC823,检测p53对肿瘤细胞的影响。结果:p53在转染细胞中表达水平提高。外源性p53的导入使肿瘤细胞增殖细胞核抗原(PCNA)水平明显降低;G0/G1期细胞数增加,S期降低。转染p53基因的MKN28细胞探鼠体内成瘤能力明显下降。结论:野生型p53基因参与调节DNA复制及细胞周期,抑制癌细胞过度增殖。Inhibitory effects of wild-type p53 on gastric cancer cell lines. Methods: Usingthe retroviral vector to introduce wild-type p53 into human gastric cancer cell line MKN28 and BGC823,The effects of p53 on these two tumor cell lines were identified. Results: Expression of p53 in transfected cell lines was increased. The introduction of exogenous wild-type p53 into tumor cells results in decreased level of proliferative cell nuclear antigen (PCNA), higher G0/G1 ratio and lower S ratio in cellcycle distribution in comparison with the control. The tumorigenicity fo MKN28 cells in nude mice wassuppressed by exogenous p53. Conclusion: p53 plays an important role in regulating DNA replicationand cell cycle, and in suppressing cell proliferation.
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