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.
Background: Even though the mechanism is unknown, previous studies have demonstrated that the traditional chemotherapy agents, 3'-azido-3'-deoxythymidine (AZT) and arsenic trioxide (As 2 O 3 ), can synergetically inhibit the growth, migration and the invasion of hepatocellular carcinoma cells. This study aimed to investigate the role which aquaglyceroporin 9 (AQP9), an arsenic channel protein which is widely distributed in the liver tissues, plays in the process of As 2 O 3 combined with AZT in inhibiting growth, migration and the invasion of hepatocellular carcinoma cells. Methods: HepG2 and MHCC97H cells were treated using As 2 O 3 (2 μM) combined with a wide range of different concentrations of AZT (0, 10, 20 μM) for 48 h, and the proliferation inhibition rates were detected using a MTT assay. AQP9 mRNA/protein expression was determined by RT-PCR and western blotting assays, respectively. Next, HepG2 cells were electro-transfected with AQP9 siRNA to disturb the expression of AQP9, which was verified by RT-PCR and western blotting. The effect of the 2 μM As 2 O 3 combined with 20 μM AZT (the optimum synergy inhibition concentration investigated previous) on the migration and invasion of HepG2 cells was then measured by wound healing assay and transwell migration assay and invasion assays, respectively, before and after an AQP9-siRNA transfection. Results: The proliferation inhibition rate from the combination of As 2 O 3 and AZT on the hepatocellular carcinoma cells was significantly higher than the rate from As 2 O 3 alone (P<0.05), and it had a greater dosedependent effect when it was compared to AZT. A low dose of As 2 O 3 (2 μM) combined with AZT (20 μM) also significantly inhibited the migration and invasion of liver cell carcinoma. The expression levels of AQP9 in the combination of As 2 O 3 (2 μM) and AZT (20 μM) group were significantly higher than those from the As 2 O 3 alone group and the blank control group (P<0.05). After silencing AQP9, the effect of the combination between As 2 O 3 and AZT for the migration and invasion of liver cell carcinoma was significantly reduced (P<0.05).Conclusions: AZT improves the efficiency of As 2 O 3 on inhibiting the proliferation, migration and invasion of hepatocellular carcinoma cells by up-regulating the expression of AQP9, which has important implications in reducing the poisonous side effect of As 2 O 3 for cancer therapies.
ContextPrevious studies have demonstrated that 3′-azido-3′-deoxythymidine (AZT) and arsenic trioxide (As2O3), traditional chemotherapy agents, can synergically inhibit the growth of hepatocellular carcinoma cells. However, the molecular mechanisms underlying As2O3 and AZT anti-hepatoma activity are unknown.ObjectiveThis study aimed to investigate the role of early growth response protein 1 (Egr-1) in the process of As2O3 combined with AZT inhibiting proliferation and inducing apoptosis of human hepatocellular carcinoma HepG2 cells, and explore the possible mechanism.Materials and methodsThe expression of Egr-1 was silenced using siRNA, and then HepG2 cells were treated with As2O3 (2 μM) and AZT (20 μM). The rates of cell inhibition and apoptosis were determined by the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) method and flow cytometry, respectively. The mRNA and protein expression of p53, caspase-3, and Egr-1 were detected by real-time quantitative polymerase chain reaction and Western blotting, respectively.ResultsThe inhibitory rate of As2O3 (2 μM) combined with AZT (20 μM) on proliferation of HepG2 cells was significantly higher than that of As2O3 alone. The combination index (CI) values were 0.2
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