层连蛋白受体67LR在胶质瘤细胞增殖中作用的研究

脑胶质瘤是颅内常见恶性肿瘤,常规的治疗手段很难将其完全治愈.67 kD层连蛋白受体(67 kDlaminin receptor,67LR)属于高亲和,非整联蛋白家族成员,试验表明,该蛋白在许多癌细胞表面过量表达,并且其表达水平与肿瘤细胞的粘附、增殖、分化、迁移、信号转导及转移能力密切相关.本试验利用shRNA干扰、RT-PCR、免疫细胞化学和MTT等技术通过下调67LR基因的表达来探讨其在胶质瘤细胞中的表达情况,及其对胶质瘤细胞增殖能力的影响.结果发现,相对于正常脑组织,67LR在脑胶质瘤细胞表面大量表达.采用shRNA下调其表达后发现胶质瘤细胞的增殖能力明显降低.结果表明,67LR在胶质瘤细胞表面的过表达与此细胞的增殖能力呈明显相关.

Down-regulation of 67LR Reduces the Migratory Activity of Human Glioma Cell

Glioma is the most common brain tumor in central nervous system.Traditional therapies are not effective to cure this disease.Experimental evidence indicates that the 67 kDa elast in laminin receptor(67LR) subunit is a high-affinity non-integrin laminin-binding protein that is over-expressed on the tumor cell surface in some kinds of cancers which plays an important role in several physiological as well as pathological processes,including cell differentiation,growth,adhesion and cancermetastatic phenotype.In this study,we testified whether 67LR was constitutively over-expressed in high-grade astrocytomas,and investigated the role of a low level of 67LR expression in glioma cell line-SHG44 by constructing an interfering RNA expression plasmid.The results showed that the 67LR had an enhanced over-expression in high-grade astrocytom as against normal brain tissues samples,and that the proliferation of glioma cells was reduced after the down-regulation of the 67LR gene by RNAi.We hypothesized that a low level of 67LR expression could reduce proliferation of glioma cells,which further proved that 67LR played an important role in glioma invasion by mediating tumor cell functions leading to sarcomata.This study provides a new alternative to gene ther apy for glioma treatment.