EMP1 regulates caspase-9 and VEGFC expression and suppresses prostate cancer cell proliferation and invasion

Abstract

This study aimed to analyze the expression, clinical significance of f epithelial membrane protejn-1 (EMP-1) in prostate carcinoma, and the biological effect in its cell line by EMP1 overexpression. Immunohistochemistry and Western blot were used to analyze EMP1 protein expression in 76 cases of prostate cancer and 34 cases of normal tissues to study the relationship between EMP1 expression and clinical factors. EMP1 lentiviral vector and empty vector were respectively transfected into prostate cancer PC-3 cell line. Quantitative real-time reverse transcription polymerase chain reaction and Western blot were used to detect the mRNA level and protein of EMP1. 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay, migration, and invasion assays were also conducted as to the influence of the upregulated expression of EMP1 that might be found on PC-3 cell biological effect. Immunohistochemistry: The level of EMP1 protein expression was found to be significantly lower in prostate cancer tissue than normal tissues (P < 0.05). Western blot: The relative amount of EMP1 protein in prostate cancer tissue was found to be significantly lower than in normal tissues (P < 0.05). The level of EMP1 protein expression was not correlated with age and prostate-specific antigen (PSA) concentration (P > 0.05), but it was correlated with T stages, lymph node metastasis, clinic stage, and Gleason score (P < 0.05). The result of biological function shown that PC-3 cell transfected EMP1 had a lower survival fraction, higher cell apoptosis, significant decrease in migration and invasion, higher caspase-9, and lower VEGFC protein expression compared with PC-3 cell untransfected EMP1 (P < 0.05). EMP1 expression decreased in prostate cancer and correlated significantly T stages, lymph node metastasis, clinic stage, and Gleason score, suggesting that EMP1 may play important roles as a negative regulator to prostate cancer PC-3 cell by regulating the expression of regulation of caspase-9 and VEGFC protein.