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作 者:李焰[1] 汪静[2] 邓敬兰[2] 吴军正[1] 李富军[2] 刘斌[1]
机构地区:[1]第四军医大学口腔医院口腔生物学教研室,西安710032 [2]第四军医大学西京医院核医学科
出 处:《中华核医学杂志》2002年第6期366-368,共3页Chinese Journal of Nuclear Medicine
基 金:国家自然科学基金资助项目 (3950 0 0 35 ;39870 2 1 8);全军医药卫生科研基金资助项目 (X0 1MB1 2 0 );第四军医大学科技创新工程资助项目 (CX99A0 1 2 )
摘 要:目的 探讨人涎腺粘液表皮样癌细胞系 (MEC 1)及人粘液表皮样癌高转移细胞株(Mc3)生长抑素受体 (SSTR) 2种亚型 (SSTR1、SSTR2 )的表达 ,及两者与SSTR的放射配基1 2 5I RC 16 0的结合差异。方法 ①采用细胞计数法、软琼脂法等观察MEC 1及Mc3细胞株生物学特性 ;②以原位杂交法检测MEC 1、Mc3细胞株SSTR1及SSTR2亚型的表达情况 ;③以放射配基结合分析法分析MEC 1、Mc3细胞与1 2 5I RC 16 0结合情况。结果 ①MEC 1、Mc3细胞生长稳定 ,Mc3细胞较MEC 1生长速度略快 ,克隆形成率高 ;②MEC 1细胞高度表达SSTR1及SSTR2 ,表达率分别为 82 .6 %和 81.7% ;Mc3细胞未见 2种亚型表达 ;③MEC 1和Mc3细胞与1 2 5I RC 16 0的特异结合率分别为 (2 3.8± 9.4 ) %和 (3.2± 2 .3) % ,差异有显著性 (P <0 .0 1)。结论 MEC 1高度表达SSTR1及SSTR2 ,其与SSTR配基RC 16 0的特异结合率显著高于Mc3细胞。ObjectiveTo study the expression of the somatostatin receptor and its binding to somatostatin analogue RC-160 in MEC-1 and Mc3 cells. MethodsHuman salivary gland mucoepidermoid carcinoma cell line MEC-1 and its highly metastatic clone Mc3 were used in this study. Cell growth was studied by cell counting and clonogenic assay, the expression of somatostatin receptor SSTR1 and SSTR2 was studied by in situ hybridization and the binding of the receptor to a somatostatin analogue RC-160 was studied by in vitro radioligand binding assay. Department of Oral Biology, Stomatological College, Fourth Military Medical University, Xi'an 710032, China AbstractObjectiveTo study the expression of the somatostatin receptor and its binding to somatostatin analogue RC-160 in MEC-1 and Mc3 cells. MethodsHuman salivary gland mucoepidermoid carcinoma cell line MEC-1 and its highly metastatic clone Mc3 were used in this study. Cell growth was studied by cell counting and clonogenic assay, the expression of somatostatin receptor SSTR1 and SSTR2 was studied by in situ hybridization and the binding of the receptor to a somatostatin analogue RC-160 was studied by in vitro radioligand binding assay. [WTHResultsThe population doubling time of MEC-1 and Mc3 cells were 30.0 and 26.4 h, clonogenecity were 1.2% and 14.2%, respectively. The expression of SSTR1 and SSTR2 in MEC-1 cells were 82.6% and 81.7%, respectively, and was nearly 0 in Mc3 cells. The specific binding of MEC-1 cells to RC-160 was much higher than that of Mc3 cells. ConclusionThe highly metastatic potential of Mc3 cells may be related to the lack of somatostatin receptor and low binding efficiency to somatostatin analogue RC-160.
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