Abstract
BACKGROUND: The poor response of patients with gliomas to existing immunotherapy has resulted in negligible improvement in prognosis. It is widely acknowledged that HBXIP serves as a transcriptional activator implicated in tumorigenesis across various cancer types. However, its specific role within glioma remains unclear. The aim of this study was to determine the association between HBXIP expression and survival and tumor-infiltrating immune cells. In addition, to construct a prognostic model to predict the overall survival (OS) of patients with glioma. METHODS: Transcriptome sequencing data of 325 patients with glioma in the Chinese Glioma Genome Atlas (CGGA) database and 702 patients with glioma in The Cancer Genome Atlas (TCGA) were included for retrospective analysis and were used as the training group and the validation group, respectively. The expression of HBXIP in pancancer was detected in the database. A t-test and one-way analysis of variance were used to determine the differential expression levels of HBXIP across distinct subgroups of glioma. Functional annotations pertaining specifically to HBXIP's biological relevance underwent scrutiny via Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. The prognostic significance of HBXIP in glioma was ascertained through Kaplan-Meier curves and Cox regression models, a nomogram was used to establish a prognostic model, and the predictive power was evaluated with calibration curves and the concordance index. HBXIP's association with inhibitory immune checkpoints and tumor immune cell infiltration was examined using Pearson correlation coefficients via Tumor Immune Estimation Resource database. RESULTS: We found that HBXIP was upregulated in glioma, and that elevated HBXIP expression correlated significantly with adverse clinicopathological features and decreased OS. Multivariate analysis showed that HBXIP was an independent prognostic biomarker for glioma, and the established prognostic model could accurately predict the OS of patients. We also found that HBXIP expression was positively correlated with inhibitory immune checkpoint expression, HBXIP overexpression was associated with increased levels of tumor immunoinfiltrating cells in glioma that resulted in poor survival, and HBXIP demonstrated a positive correlation with the expression of immune cell marker genes. CONCLUSIONS: HBXIP is closely related to the clinicopathologic factors in glioma and may function as an oncogene. Its high expression is associated with poor prognosis, which may potentially be linked to immune escape and immune cell infiltration. HBXIP is a potential biomarker of prognostic and immune infiltration in glioma.