Abstract
Background: Old age has been demonstrated to be a risk factor for GBM, but the underlying biological mechanism is still unclear. We designed this study intending to determine a mechanistic explanation for the link between age and pathogenesis in GBM.Results: The expression of RPP30, an independent prognostic factor in GBM, was negatively correlated with age in both tumor and non-tumor brain samples. However, the post-transcriptional modifications carried out by RPP30 were different in primary GBM and non-tumor brain samples. RPP30 affected protein expression of cancer pathways by performing RNA modifications. Further, we found that RPP30 was related to drug metabolism pathways important in GBM. The decreased expression of RPP30 in older patients might be a pathogenic factor for GBM.Conclusion: This study revealed the role of RPP30 in gliomagenesis and provided the theoretical foundation for targeted therapy.Methods: In total, 616 primary GBM samples and 41 non-tumor brain samples were enrolled in this study. Transcriptome data and clinical information were obtained from the CGGA, TCGA, and GSE53890 databases. Gene Set Variation Analysis and Gene Ontology analyses were the primary analytical methods used in this study. All statistical analyses were performed using R.
Highlights
Glioblastoma (GBM) is the most common primary intracranial malignancy in adults [1, 2]
We speculated that the accumulation of gene mutations with age was the main cause of gliomagenesis
Our results suggested that the number of gene mutations does not accumulate with age in samples from the TCGA (Supplementary Figure 1A–1C) and CGGA (Supplementary Figure 1D–1F) databases
Summary
Glioblastoma (GBM) is the most common primary intracranial malignancy in adults [1, 2]. It is highly lethal, with a median survival of only about 14.4 months [3]. Results: The expression of RPP30, an independent prognostic factor in GBM, was negatively correlated with age in both tumor and non-tumor brain samples. The post-transcriptional modifications carried out by RPP30 were different in primary GBM and non-tumor brain samples. The decreased expression of RPP30 in older patients might be a pathogenic factor for GBM. Methods: In total, 616 primary GBM samples and 41 non-tumor brain samples were enrolled in this study.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
