摘要
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
Purpose:To study the status of the tumor supperessor gene locus INK4a ARF in human lung cancer cells and assess its relationship with the carcinogenesis of lung cancer.Methods:With RT PCR and Western blot,we examined the INK4a ARF gene expression status of 6 lung cancer cell lines (SPC A 1,Calu 1,H446,SH77,A549,H460),on both the mRNA and the protein levels,and the PCR products were sequenced and analyzed.Results:p16INK4a mRNA was undetectable in 3 of these cell lines (H460,Calu 1,A549),while p14ARF was simultaneously missing in H460 and A549,two adenocarcinomas,but still expressed in Calu 1, a squamous cell carcinoma.The p14ARF protein of H460 and A549 were also negative with the Western blot analysis. Conclusions:Like p16INK4a,p14ARF gene is also one of the targets of inactivation in human lung cancer. The finding is a good evidence for the relationship between carcinogenesis and the loss of p14ARF p53 pathway which is considered as an important mechanism of self protection in cells.
出处
《中国癌症杂志》
CAS
CSCD
2000年第1期15-18,共4页
China Oncology
基金
上海市科委研究基金项目! (编号 9741190 3 7)