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目的 :研究抑癌基因位点INK4a ARF在肺肿瘤细胞中的表达状况 ,揭示p14ARF和p16INK4a协同表达缺失与肺癌发生发展的相关性。方法 :用RT PCR和Westernblot对 6株肺癌细胞 (SPC A 1,Calu 1,H44 6 ,SH77,A5 49,H46 0 )的INK4a ARF基因位点在mRNA、蛋白质水平上进行检测 ,对PCR产物进行纯化和测序分析。结果 :6株肺癌细胞中 ,有 3株细胞 (H46 0 ,Calu 1,A5 49)的p16INK4a基因表达缺失 ,其中 ,Calu 1表达正常p14ARF的mRNA ,而在H46 0和H5 49这两株非小细胞肺癌中 ,p14ARF和p16INK4a发生协同表达缺失。结论 :p14ARF基因与p16INK4a一样 ,是肺肿瘤细胞中的失活靶点之一。揭示了p14ARF缺失导致p5 3保护机制失效与肺癌的相关性
Objective : To study the expression status of tumor suppressor gene INK4a ARF in lung tumor cells, and to reveal the correlation between the lack of coexpression of p14ARF and p16INK4a and the development of lung cancer. METHODS: The INK4a ARF gene loci in six lung cancer cells (SPC A 1, Calu 1, H44 6, SH77, A5 49, H46 0) were detected by RT PCR and Western blot at the mRNA and protein levels, and PCR products were analyzed. Purification and sequencing analysis. RESULTS: Of the 6 lung cancer cells, 3 cells (H46 0, Calu 1, A5 49) lacked p16INK4a gene expression. Among them, Calu 1 expressed normal p14ARF mRNA, while the H46 0 and H5 49 strains were not small. In lung cancer, p14ARF and p16INK4a have a synergistic loss of expression. Conclusion : The p14ARF gene, like p16INK4a, is one of the targets of inactivation in lung tumor cells. Reveals that the p14ARF deletion leads to failure of the p53 protection mechanism and its association with lung cancer