Background: Long noncoding RNAs play influential roles in the progression of many types of human malignancies. The present study aimed to explore the prognostic value of long noncoding RNA FTX (FTX) on patients with glioma. Methods: FTX expression in glioma specimens and matched adjacent non-neoplasm specimens was examined by a quantitative real-time polymerase chain reaction assay. Furthermore, assays of the relationships between FTX expression and clinicopathologic characteristics of patients with glioma were also performed. Kaplan-Meier methods were applied for the assays of the overall survival (OS) and progression-free survival (PFS) of patients and Cox regression assays were used to analyze the clinical value of FTX used as a possible biomarker. Results: FTX levels were significantly up-regulated in glioma specimens compared to the paired non-neoplasm specimens (p < 0.01). Furthermore, high FTX expression in neoplasm tissues was dramatically associated with World Health Organization grade (p = 0.001) and Karnofsky Performance Score (p = 0.009). Kaplan-Meier assays with 187 patients revealed that patients with high level of FTX expression displayed poorer OS (p = 0.002) and PFS (p = 0.000). Subsequently, multivariable Cox regression analysis identified FTX expression as an independent prognostic factor of unfavorable survivals in glioma (OS: p = 0.001; PFS: p = 0.002). Conclusions: These findings indicated that FTX may be a novel predictor for prognostic assessment of glioma patients. However, studies conducted with larger numbers of patients are essential to confirm our findings.
Malignant glioma is the most common primary brain carcinoma in the world and has a poor survival rate. Previous studies have demonstrated that p53 dysfunction contributes to the development and severity of malignant glioma. It has also been demonstrated that Newcastle disease virus (NDV) may be a viable candidate for the treatment of various types of cancer. In the present study, a p53 oncolytic agent delivered using recombinant NDV (rNDV-p53) was constructed and its anti-tumor effects and were assessed. Glioma cell lines and a xenograft mouse model were utilized to assess the ability of p53 and rNDV to promote apoptosis and induce immunotherapy, respectively. The mechanism of rNDV-p53 in glioma therapy was investigated using quantitative polymerase chain reaction and immunohistochemistry. Tumor-specific cytotoxic T-lymphocyte (CTL) responses and lymphocyte infiltration were also analyzed in glioma-bearing models. The results of the present study demonstrate that rNDV-p53 may be a potential therapeutic agent that improves the prognosis of mice with glioma. It was revealed that rNDV-p53 inhibits glioma cell growth and aggressiveness and compared with rNDV and p53 alone. The results also demonstrated that rNDV-p53 induced glioma cell apoptosis by upregulating apoptosis-related genes. In addition, the present study demonstrated that rNDV-p53 significantly stimulated CTL responses and lymphocyte infiltration whilst increasing the number of apoptotic bodies . Furthermore, rNDV-p53 therapy inhibited tumor regression and prolonged the survival of glioma-bearing mice. In conclusion, rNDV-p53 invoked an immune response against glioma cells, which may serve as a comprehensive immunotherapeutic schedule for glioma.
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