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6A8 α—甘露糖苷酶表达低下致人鼻咽癌细胞CNE—2L2生长抑制
作者姓名:Yue W  Shi GX  Bai ZL  Zhu LP
作者单位:中国医学科学院,中国协和医科大学,基础医学研究所免疫学系,北京,100005
基金项目:国家自然科学基金重点项目(39630300)资助
摘    要:目的:研究6A8 α-甘露糖苷酶与CNE-2L2肿瘤细胞生长的关系。方法:用腺相关病毒载体将反义6A8 cDNA导入鼻咽癌细胞CNE-2L2。细胞中6A8 α-甘露糖苷酶表达情况用单抗6A8a免疫荧光染色、α-甘露糖苷酶添生及ConA结合试验检测。以野生型细胞、转导了空载体或正义6A8的细胞作对照,以MTT、集落形成及裸鼠实验检测肿瘤细胞生长。结果:转导反义6A8能抑制CNE-2L2细胞6A8 α-甘露糖苷酶表达,6A8 α-甘露糖苷酶表达抑制的CNE-2L2细胞的MTT值、形成集落数及接种裸鼠皮下后所长肿瘤的重量均较对照显著降低可减小(P<0.001)。结论:6A8 α-甘露糖苷酶表达低下致人鼻咽癌细胞CNE-2L2生长抑制。

关 键 词:6A8  α-甘露糖苷酶  CNE-2L2细胞  肿瘤生长  鼻咽癌
修稿时间:2001年3月27日

Growth inhibition of human nasopharyngeal carcinoma cell CNE-2L2 caused by suppression of 6A8 alpha-mannosidase expression
Yue W,Shi GX,Bai ZL,Zhu LP.Growth inhibition of human nasopharyngeal carcinoma cell CNE-2L2 caused by suppression of 6A8 alpha-mannosidase expression[J].Acta Academiae Medicinae Sinicae,2001,23(5):418-422.
Authors:Yue W  Shi G X  Bai Z L  Zhu L P
Institution:Department of Immunology, Institute of Basic Medical Sciences, CAMS, PUMC, Beijing 100005, China.
Abstract:OBJECTIVE: To study the relationship between 6A8 alpha-mannosidase expression and growth of CNE-2L2 cells, a human nasopharyngeal carcinoma cell line. METHODS: Recombinant adeno-associated virus vector (rAAV) was used as a mediator to transfer an antisense or a sense fragment of 6A8 cDNA into CNE-2L2 cells. 6A8 alpha-mannosidase expression was detected by means of mAb 6A8a staining, alpha-mannosidase activity assay and ConA binding test. Cell growth was examined by means of MTT and colony formation. Tumor growth at the inoculated site of the cells in nude mice was detected after 8 weeks. RESULTS: Transduction of antisense 6A8 could reduce the expression of 6A8 alpha-mannosidase. In comparison to those in controls, the wild type, the mock-transduced and the sense 6A8-transduced cells, the MTT value, the colony number formed and the tumor weight grown at the inoculated site of cells were significantly decreased in the antisense 6A8-transduced cells (P < 0.001). CONCLUSION: Decreased expression of 6A8 alpha-mannosidase caused an inhibition of CNE-2L2 cell growth.
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