High Hepatic leukemia factor expression indicates a favorable survival in glioma patients.

Abstract

Hepatic leukemia factor (HLF) is an oncogenic transcript factor, but its role in gliomas is unclear.With the open-access data from the Cancer Genome Atlatls (TCGA), HLF expression was compared between normal and glioma tissues and its correlation to patient survival, age, gender, race, and tumor grade was analyzed. Multivariate Cox regression was adopted to explore the independent risk factors for patient survival. Survivals between high and low HLF expression, and high and low model predicted risk subgroups were compared. 1, 2, 3, and 5-year patient survival were predicted with the Cox regression model. Gene set enrichment analysis (GSEA) was performed to predict the potential function of HLF.Expression and clinical data of 5 normal brain samples and 655 glioma samples were obtained from TCGA. HLF expression was downregulated in gliomas than normal brain tissue (P = .007), and negatively related to patient age and advancing tumor grade (P < .001). HLF was a protective factor for patient survival (OR = 0.81, 95%CI 0.67–0.99, P = .035). Patients’ survivals were poorer in low HLF expression subgroups and the Cox regression model predicted high-risk subgroups (P < .001). The accuracy of the model in predicting 1, 2, 3, and 5-year patient survival was 0.864, 0.895, 0.907, and 0.893, respectively. GSEA revealed HLF mainly took part in regulating tumor cell metabolism and cell cycle.HLF was downregulated in gliomas than normal tissue, negatively related to patient age and tumor grade, and was an independent protective factor for glioma patients.