CENPN Acts as a Novel Biomarker that Correlates With the Malignant Phenotypes of Glioma Cells

• Main Authors: Hailong Wu, Yan Zhou, Haiyang Wu, Lixia Xu, Yan Yan, Xiaoguang Tong, Hua Yan
• Format: Article
• Language: English
• Published: Frontiers Media S.A. 2021-09-01
• Series: Frontiers in Genetics
• Subjects: CENPN; biomarker; bioinformatics analysis; glioma; immune infiltration
• Online Access: https://www.frontiersin.org/articles/10.3389/fgene.2021.732376/full

Background: Gliomas are the most common intracranial malignant neoplasms and have high recurrence and mortality rates. Recent literatures have reported that centromere protein N (CENPN) participates in tumor development. However, the clinicopathologic significance and biological functions of CENPN in glioma are still unclear.Methods: Clinicopathologic data and gene expression profiles of glioma cases downloaded from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) databases were utilized to determine the associations between the expression of CENPN and clinical features of glioma. Kaplan-Meier and ROC curves were plotted for prognostic analysis. Gene set enrichment analysis (GSEA) and single sample gene set enrichment analysis (ssGSEA) were applied to identify immune-related functions and pathways associated with CENPN’ differential expression. In vitro experiments were conducted to investigate the impacts of CENPN on human glioma cells.Results: Elevated CENPN expression was associated with unfavorable clinical variables of glioma patients, which was validated in clinical specimens obtained from our institution by immunohistochemical staining (IHC). The GSEA and ssGSEA results revealed that CENPN expression was strongly correlated with inflammatory activities, immune-related signaling pathways and the infiltration of immune cells. Cell experiments showed that CENPN deficiency impaired cell proliferation, migration and invasion ability and increased glioma apoptosis.Conclusion: CENPN could be a promising therapeutic target for glioma.