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TP53I13 promotes metastasis in glioma via macrophages, neutrophils, and fibroblasts and is a potential prognostic biomarker
Ge, Xinqi1,2; Xu, Manyu1,2; Cheng, Tong1,2; Hu, Nan2; Sun, Pingping1; Lu, Bing1; Wang, Ziheng1,3,4; Li, Jian3
2022-10-07
Source PublicationFrontiers in Immunology
ISSN1664-3224
Volume13Pages:974346
Abstract

Background: TP53I13 is a protein coding tumor suppression gene encoded by the tumor protein p53. Overexpression of TP53I13 impedes tumor cell proliferation. Nevertheless, TP53I13 role and expression in the emergence and progression of glioma (low-grade glioma and glioblastoma) are yet to be identified. Thus, we aim to use comprehensive bioinformatics analyses to investigate TP53I13 and its prognostic value in gliomas. Methods: Multiple databases were consulted to evaluate and assess the expression of TP53I13, such as the Cancer Genome Atlas (TCGA), the Chinese Glioma Genome Atlas (CGGA), GeneMANIA, and Gene Expression Profiling Interactive. TP53I13 expression was further explored using immunohistochemistry (IHC) and multiplex immunohistochemistry (mIHC). Through Gene Set Enrichment Analysis (GSEA), the biological functions of TP53I13 and metastatic processes associated with it were studied. Results: The expression of TP53I13 was higher in tumor samples compared to normal samples. In samples retrieved from the TCGA and CGGA databases, high TP53I13 expression was associated with poor survival outcomes. The analysis of multivariate Cox showed that TP53I13 might be an independent prognostic marker of glioma. It was also found that increased expression of TP53I13 was significantly correlated with PRS type, status, 1p/19q codeletion status, IDH mutation status, chemotherapy, age, and tumor grade. According to CIBERSORT (Cell-type Identification by Estimating Relative Subsets of RNA Transcript), the expression of TP53I13 correlates with macrophages, neutrophils, and dendritic cells. GSEA shows a close correlation between TP53I13 and p53 signaling pathways, DNA replication, and the pentose phosphate pathway. Conclusion: Our results reveal a close correlation between TP53I13 and gliomas. Further, TP53I13 expression could affect the survival outcomes in glioma patients. In addition, TP53I13 was an independent marker that was crucial in regulating the infiltration of immune cells into tumors. As a result of these findings, TP53I13 might represent a new biomarker of immune infiltration and prognosis in patients with gliomas.

KeywordCgga Cibersort Ihc Immune Infiltration Tcga Tme Tp53i13
DOI10.3389/fimmu.2022.974346
URLView the original
Indexed BySCIE
Language英語English
WOS Research AreaImmunology
WOS SubjectImmunology
WOS IDWOS:000874695000001
Scopus ID2-s2.0-85140346700
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Document TypeJournal article
CollectionCentre for Precision Medicine Research and Training
Corresponding AuthorWang, Ziheng; Li, Jian
Affiliation1.Department of Clinical Biobank & Institute of Oncology, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, China
2.Medical School of Nantong University, Nantong, China
3.Department of Neurosurgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, China
4.Centre for Precision Medicine Research and Training, Faculty of Health Sciences, University of Macau, Macau SAR, China
Corresponding Author AffilicationFaculty of Health Sciences
Recommended Citation
GB/T 7714
Ge, Xinqi,Xu, Manyu,Cheng, Tong,et al. TP53I13 promotes metastasis in glioma via macrophages, neutrophils, and fibroblasts and is a potential prognostic biomarker[J]. Frontiers in Immunology, 2022, 13, 974346.
APA Ge, Xinqi., Xu, Manyu., Cheng, Tong., Hu, Nan., Sun, Pingping., Lu, Bing., Wang, Ziheng., & Li, Jian (2022). TP53I13 promotes metastasis in glioma via macrophages, neutrophils, and fibroblasts and is a potential prognostic biomarker. Frontiers in Immunology, 13, 974346.
MLA Ge, Xinqi,et al."TP53I13 promotes metastasis in glioma via macrophages, neutrophils, and fibroblasts and is a potential prognostic biomarker".Frontiers in Immunology 13(2022):974346.
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