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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 elastin-laminin receptor (67LR) subunit is a high-affinity non-integrin laminin-binding protein that is over-expressed on the tumor cell surface in a variety of cancers and plays an important role in several physiological as well as pathological processes,including cell differentiation,growth,migration and cancer invasion.In this study,we testified whether 67LR was constitutively over-expressed in high-grade astrocytomas,and then investigated the role of a low level of 67LR expression in glioma cells by constructing an interfering RNA expression plasmid.The results showed that the 67LR was constitutively overexpressed in high-grade astrocytomas and glioma cells reduced their migratory activity after interference of the 67LR expression by RNAi.We hypothesized a low level of 67LR expression could reduced migtratoty activity of glioma cell,which further proved that 67LR played an important role in tumor invasion by mediating essential tumor cell functions leading to metastases.This study provides a new alternative to gene therapy for glioma treatment.