鼻咽癌细胞株SUNE-1异质性分子机制的研究

Study on the molecular mechanisms of tumor heterogeneity of nasopharyngeal carcinoma cell line SUNE-1

目的 从病毒和遗传两方面探讨鼻咽癌细胞株 SUNE- 1三亚株 :5 - 8F(高成瘤、高转移 )、6 - 10 B(只成瘤、不转移 )和 13- 9B(不成瘤 )异质性的分子机制。方法 (1)应用原位杂交技术检测 SU NE- 1及其三亚株中 EBV-L MP1的表达状况 ;(2 )应用 CGH检测 SUNE- 1及其三亚株的基因扩增情况。结果 (1)在三亚株中 ,都能够检测到 EBV- L MP1的表达。 (2 ) CGH检测发现 SUNE- 1的 DNA拷贝数变呈现以 1、2 p、3、4、5 p、6、7、9、10 q、11、12 q、13q、17q和 18q增加和 2 2 q拷贝数减少为主 ;5 - 8F染色体变化以 3p、7q、8q、9q和 10 q拷贝数增加为主 ;而 6 - 10 B和13- 9B除少数几个染色体区域发生缺失外 ,均无 DNA拷贝数的增加。结论 鼻咽癌细胞株 SU NE- 1及其三亚株 ,均有 EBV的表达和存在不同的基因变化 ,提示其异质性可能主要由于基因的变化引起 ,但 EBV对维持鼻咽癌的恶性程度起着重要的作用。

Objective To investigate the molecular mechanisms of tumor heterogeneity of nasopharygeal carcinoma cell line (SUNE-1) and its three sublines. Method (1)Determing the expression of EBV-LMP1 in the sublines using in situ hybrization.(2)Molecular cytogentic analysis of the cell line and sublines by CGH. Results (1)Expression of LMP1 was observed in the SUNE-1 and its three sublines. (2)There were DNA copy number gains on chromosomes 1,2p,3,4,5p,6,7,9,10q,11,12q,13q,and 18q as well as loss on 22q in the SUNE-1 cell line;DNA copy number gains on chromosomes 3p,7q,8q,9q,and 10q were observed in 5-8F subcline;DNA copy number loss on few chromosomes,but no DNA copy number gain was observed in the 6-10B and 13-9B subclines. Conclusion The tumor hetergeneity of the SUNE-1 and its three subclines may be due to genetic changes,and EBV infection may be maintain the malignant phenotypic of nasopharygeal carcinoma.\;