中文摘要：

目的探讨过表达LRIG3基因对神经胶质瘤细胞株U251与U87增殖及增殖细胞核抗原（PCNA）和Ki-67表达的影响及其机制。方法用携带LRIG3过表达特异性序列和只含空白载体的质粒用慢病毒法感染胶质瘤细胞株U251与U87，筛选稳定株，分别分成实验组和对照组，通过逆转录．聚合酶链反应（RT—PCR）和Westernblot法检测各组细胞LRIG3表达的变化，应用噻唑蓝（MTr）比色法检测病毒感染后对胶质瘤细胞株U251与U87增殖的影响，用免疫组织化学链霉亲和素生物素复合物（SABC）法分别检测各组细胞中PCNA和Ki-67的表达差异。结果LRIG3过表达组细胞中LRIG3mRNA水平与对照组比较分别升高67．6％（U251）和79．9％（U87），LRIG3蛋白表达水平分别升高62．3％（U87）和91．0％（U251）。MTF法结果显示两实验组细胞增殖率均低于相应对照组。U251细胞对照组PCNA阳性率为（47．81±4．67）％，实验组为（27．49±3．17）％，U87细胞对照组PCNA阳性率为（55．50±4．01）％，实验组为（33．60±4．82）％，差异均有统计学意义（P〈0．05）。U251细胞对照组中Ki-67的阳性率为（48．50±6．11）％，实验组为（24．30±3．76）％，U87细胞对照组Ki-67阳性率为（55．20±4．19）％，实验组为（23．50±4．60）％，差异均有统计学意义（P〈0．01）。结论LRIG3基因过表达可减少胶质瘤细胞的增殖。

英文摘要：

Objective To explore the effect of overexpression of LRIG3 gene on proliferation of glioma cells and expression of proliferating cell nuclear antigen （PCNA） and Ki-67, and the possible mecbanisms. Methods The plasmid containing LRIG3 gene and control was transduced into glioma U251 and U87 cells respectively. The mRNA and protein levels of LRIG3 were detected by using reverse tran- scription-polymerase chain reaction （RT-PCR） and Western blotting. Cell proliferation was examined by methyl thiazol tetrazolium （MTI＇） assay. The expression of PCNA and Ki-67 was detected by strept avidinbiotin complex （SABC）. Results Compared with control cells, the mRNA levels of LRIG3 were raised by 67.6% and 79. 9% in LRIG3 cells of U87 and U251, respectively, and the protein levels were increased by 62. 3% （U87） and 91.0% （ U251 ） respectively. Overexpression of LRIG3 resulted in the reduction of cell proliferation. The positive rate of PCNA was significantly lower in LRIG3 cells than in control ceils [U87：（33.60 ±4. 82）% vs （55.50 ±4. 01）% ; U251 ： （27. 49 ±3.17）% vs （47. gl ±4. 67）% （P 〈 0. 05 ） ]. The positive rate of Ki-67 was also significantly decreased in LRIG3 transduced cells as compared with control cells [ U87 ： （23.50 ±4. 60） % vs （55.20 ±4. 19） % ; U251 ： （24. 30 ± 3.76） % vs （48. 50 ± 6. 11 ） % （P 〈 0. 01 ） ]. Conclltsion Up-regulating LRIG3 gene expression can reduce the proliferation of glioma U87 and U251 ceils.