Absent expression of FLNA is correlated with poor prognosis of nasopharyngeal cancer

This study aimed to analyze the expression, clinical significance of filamin A (FLNA) in nasopharyngeal carcinoma, and the biological effect in its cell line by FLNA overexpression. Immunohistochemistry and western blot were used to analyze FLNA protein expression in 63 cases of nasopharyngeal cancer and 21 cases of normal tissues to study the relationship between FLNA expression and clinical factors. FLNA lentiviral vector and empty vector were respectively transfected into nasopharyngeal cancer CNE2 cell line. Reverse transcription–polymerase chain reaction (RT-PCR) and western blot were used to detect the mRNA level and protein of FLNA. 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide, migration, and invasion assays were also conducted as to the influence of the upregulated expression of FLNA that might be found on CNE2 cell biological effect. Immunohistochemistry: the level of FLNA protein expression was found to be significantly lower in nasopharyngeal cancer tissue than normal tissues (P < 0.05). Western blot: the relative amount of FLNA protein in nasopharyngeal cancer tissue was found to be significantly lower than in normal tissues (P < 0.05). The level of FLNA protein expression was correlated with T stages, lymph node metastasis, clinic stage, and histological grade (P < 0.05). Loss of FLNA expression correlated significantly with poor overall survival time by Kaplan–Meier analysis (P < 0.05). The result of biological function has shown that CNE2 cell-transfected FLNA had a lower survival fraction, significant decrease in migration and invasion, and lower matrix metallopeptidase 9 (MMP-9) protein expression compared with CNE2 cell-untransfected FLNA (P < 0.05). FLNA expression decreased in nasopharyngeal cancer and correlated significantly lymph node metastasis, clinic stage, histological grade, and poor overall survival, suggesting that FLNA may play important roles as a negative regulator to nasopharyngeal cancer CNE2 cell by promoting degradation of MMP-9.