Abstract
BackgroundIn cancer, kappa B-interacting protein (IKBIP) has rarely been reported. This study aimed at investigating its expression pattern and biological function in brain glioma at the transcriptional level.MethodsWe selected 301 glioma patients with microarray data from CGGA database and 697 glioma patients with RNAseq data from TCGA database. Transcriptional data and clinical data of 998 samples were analyzed. Statistical analysis and figure generating were performed with R language.ResultsWe found that IKBIP expression showed positive correlation with WHO grade of glioma. IKBIP was increased in isocitrate dehydrogenase (IDH) wild type and mesenchymal molecular subtype of glioma. Gene ontology analysis demonstrated that IKBIP was profoundly associated with extracellular matrix organization, cell–substrate adhesion and response to wounding in both pan-glioma and glioblastoma. Subsequent gene set enrichment analysis revealed that IKBIP was particularly correlated with epithelial-to-mesenchymal transition (EMT). To further elucidate the relationship between IKBIP and EMT, we performed gene set variation analysis to screen the EMT-related signaling pathways and found that IKBIP expression was significantly associated with PI3K/AKT, hypoxia and TGF-β pathway. Moreover, IKBIP expression was found to be synergistic with key biomarkers of EMT, especially with N-cadherin, vimentin, snail, slug and TWIST1. Finally, higher IKBIP indicated significantly shorter survival for glioma patients.Conclusions IKBIP was associated with more aggressive phenotypes of gliomas. Furthermore, IKBIP was significantly involved in EMT and could serve as an independent prognosticator in glioma.
Highlights
Gliomas account for the most common and aggressive primary brain cancers among adult patients [1]
We investigated the transcriptional expression profiles of I kappa B kinase interacting protein (IKBIP) in 998 glioma patients and revealed that IKBIP expression showed significant positive correlation with the WHO grade of glioma
Higher IKBIP expression indicated a significantly shorter survival for patients with glioma, across different WHO grades. These findings suggested that IKBIP played a vital role in the malignant progression of gliomas, in line with the results of a previous weighted gene co-expression network analysis (WGCNA) study [7]
Summary
Gliomas account for the most common and aggressive primary brain cancers among adult patients [1]. Despite great advances in diagnosis and treatment, the prognosis for glioma patients remains unfavorable. For those with glioblastoma (GBM), the most devastating type, the median survival time is only about 15 months [2,3]. Epithelial-to-mesenchymal transition (EMT) has been widely reported as a key mechanism in promoting migration, invasion and tumor progression in glioma [4]. We know that this gene promotes the function of apoptosis. IKBIP was found to be one of the target genes of p53 and plays a crucial role in proapoptotic function [5]. Heretofore, the biological function of IKBIP in malignancies has been rarely reported. The role of IKBIP in glioma still remains largely unclear. We took advantage of 998 glioma patients with transcriptome data to investigate
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