Syntenin is expressed in human gliomas and may correlate with tumor migration

Invasion is usually recognized as the main reason for the high recurrence and death rates of gliomas. Therefore, properly understanding the molecular mechanisms of migration and invasion of human gliomas has become a focus and will be helpful for the treatment of gliomas. Syntenin has been demonstrated to be implicated in the migration, invasion and metastasis of many types of malignant tumors. Therefore, we investigated the expression of syntenin in human gliomas and its relationship with glioma migration.

Immunohistochemistry, Western blot and real time-polymerase chain reaction (RT-PCR) were performed to detect the expression of syntenin in human gliomas. Phosphorylated FAK in human gliomas was examined by western blot.

Scattered syntenin positive glioma cells were detected by immunohistochemistry in normal tissue. Syntenin expression in grade II, III and IV gliomas increased with the degree of tumor malignancy, and no syntenin expression was detected in grade I gliomas. The level of phosphorylated FAK at the tyrosine 397 site also elevated with the degree of tumor malignancy. There was a positive correlation between the syntenin level and the pathological grade of gliomas (r s = 0.896, p < 0.05). Phosphorylated FAK was also upregulated along with the stage of glioma progression and the increase of syntenin expression.

Our results indicate that the enhanced expression of syntenin and phosphorylated FAK may correlate with the increase of the malignancy of human gliomas. Syntenin may promote human glioma migration through interaction with FAK.