Objective To detect the expression of EIF5A2 in hepatocellular carcinoma(HCC) and to explore its relation with clinicopathological characters and prognosis of HCC patients. Methods The expression of EIF5A2 mRNA and protein in 12 pairs of fresh HCC and corresponding non-tumor tissues adjacent to the cancer was examined by qRT-PCR and Western blot. The expression level of EIF5A2 in 284 pairs of HCC and adjacent non-tumor tissues was detected by IHC staining. Then we analyzed between EIF5A2 expression and clinical pathological parameters and prognosis of HCC patients. Results The relative expression levels of EIF5A2 mRNA and protein in fresh HCC tissues were significantly higher than those in the corresponding adjacent non-tumor tissues (t=5.305, P=0.0003; t=10.120, P < 0.001); EIF5A2 expression in 284 HCC tissues was significantly higher than that in the corresponding adjacent non-tumor tissues (z=-12.186, P < 0.001). The expression of EIF5A2 was significantly correlated with tumor size (χ²=13.079, P < 0.001), tumor multiplicity (χ²=4.589, P=0.032) and differentiation degree (χ²=4.844, P=0.028). The 3- and 5-year overall survival time and disease-free survival time of the patients with high expression of EIF5A2 were significantly shorter than those with low expression of EIF5A2 (P < 0.001). EIF5A2 was an independent prognostic factor affecting the 3- and 5-year overall survival time and disease-free survival time of HCC patients (P < 0.05). Conclusion The up-regulation of EIF5A2 expression may be related with the occurrence and development of hepatocellular carcinoma. The high expression of EIF5A2 is an independent influence factor for poor prognosis and EIF5A2 can be used as a potential molecular marker for predicting the prognosis of HCC patients.

Fibroblast growth factors (FGF) are a group of structurally related polypeptides which constitute an elaborate signaling system with their receptors. Evidence accumulated in the years suggests that the FGF family plays a key role in the repair of central nervous system injury. The main protective mechanisms include activating the expression of PI3K-Akt, peroxisome proliferator-activated receptor (PPARγ) and other signals; inhibiting NF-κB-mediated inflammatory response, oxidative stress and apoptosis; regulating neuronal differentiation and neuronal excitability as well as participating in protection of neurovascular units and nerve function repair. This paper comprehensively summarizes the latest research progress in FGF signaling related to diseases of the central nervous system such as cerebral infarction, cerebral hemorrhage, traumatic brain injury, Alzheimer's disease, Parkinson's disease, epilepsy and depression, aiming to provide scientific basis and reference for the development of innovative FGF drugs for the prevention and treatment of neurological diseases.
Humans ; Fibroblast Growth Factors ; Phosphatidylinositol 3-Kinases/metabolism* ; Central Nervous System/metabolism* ; Signal Transduction/physiology* ; Alzheimer Disease