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背景与目的:p53基因突变是肺腺癌发生中的常见的分子生物学事件,第245位点突变为其突变热点之一,因此研究p53基因第245位点突变可能为肺腺癌的诊断、治疗提供一定的理论基础。本研究旨在研究肺癌常见的245位点突变对p53缺失的人肺腺癌细胞系H1299的影响。方法:应用流式细胞术观察脂质体瞬时转染p53基因第245突变体(G245V)对细胞凋亡的影响,同时用稳定转染观察克隆形成率和生长曲线的不同。结果:转染G245V突变体的H1299细胞凋亡平均数低于转染野生型p53基因的细胞,差异有统计学意义(P<0.001);大中克隆形成数量比导入野生型p53基因的细胞大中克隆形成数量明显增多,差异有统计学意义(P<0.05);细胞的生长速度也明显加快。结论:p53基因第245位点发生突变后基本丧失了野生型p53的功能,是肿瘤细胞增殖的原因之一。
BACKGROUND & OBJECTIVE: The p53 gene mutation is a common molecular biological event in the development of lung adenocarcinoma. The mutation at position 245 is one of the hot spots. Therefore, to study the mutation at position 245 of p53 gene may be the diagnosis of lung adenocarcinoma, Treatment provides a certain theoretical basis. The purpose of this study was to investigate the effect of a common 245 site mutation in lung cancer on p53-deficient human lung adenocarcinoma cell line H1299. Methods: Flow cytometry was used to observe the effect of G245V transient transfection on the apoptosis of p53 cell line. The stable transfection was used to observe the difference of colony formation rate and growth curve. Results: The average number of apoptosis of H1299 cells transfected with G245V mutant was lower than that of wild type p53 gene transfected cells (P <0.001). The number of large and medium clone formation was larger than that of wild type p53 gene The number of middle clones was significantly increased (P <0.05), and the growth rate of the cells was also significantly accelerated. Conclusion: The mutation of p53 site at position 245 basically lost the function of wild type p53, which is one of the reasons of tumor cell proliferation.