{"title":"Diagnostics and immunological function of CENPN in human tumors: from pan-cancer analysis to validation in breast cancer.","authors":"Yubo Jing, Yiyang Wang, Yongxiang Li, Xinzhu Huang, Junyi Wang, Dlraba Yelihamu, Chenming Guo","doi":"10.21037/tcr-24-1291","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Centromere protein N (<i>CENPN</i>), a member of the centromere protein family, contributes to ribonucleic assembly, mitosis progression, and chromosome separation. <i>CENPN</i> manifests a close link with the occurrence and progression of several malignant cancers, but there is no pan-cancer study on <i>CENPN</i>, and we aim to ascertain the connection between <i>CENPN</i> and human cancer prognosis and immunotherapy.</p><p><strong>Methods: </strong>The <i>CENPN</i> function in multiple malignant tumors was comprehensively investigated with data from The Cancer Genome Atlas (TCGA) and integrated Gene Expression Omnibus (GEO) database. We examined the transcriptional level, prognostic effect, diagnostic value, genetic and epigenetic alteration, methylation level, and immunological importance of <i>CENPN</i>. Furthermore, this work provided further confirmation of the phenotypic regulating function of <i>CENPN</i> in breast cancer (BC) cells.</p><p><strong>Results: </strong><i>CENPN</i> exhibited significant upregulation in diverse cancer tissues and had different expression patterns across immunological and molecular subgroups in several cancer types. Elevated expression of <i>CENPN</i> may correlate with a worse prognosis. <i>CENPN</i> effectively differentiates most cancers from healthy tissues. Hypomethylate was shown to be <i>CENPN</i> promoter in most cancers. <i>CENPN</i> was shown to be connected with levels of different immune cell infiltration. Kyoto Encyclopedia of Genes and Genomes (KEGG) and the Gene Set Enrichment Analysis (GSEA) analysis suggested that <i>CENPN</i> may mediate neutrophil extranuclear trap formation, cell cycle, and P53 signaling pathways in cancer. <i>In vitro</i> studies showed that the overexpression of <i>CENPN</i> promotes the proliferation, invasion, and migration of BC cells, while concurrently inhibiting their apoptosis.</p><p><strong>Conclusions: </strong><i>CENPN</i> may operate as a novel predictive indicator and molecular target for targeted therapy in pan-cancer. Significantly, <i>CENPN</i> contributed to controlling the BC growth and advancement.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 2","pages":"881-906"},"PeriodicalIF":1.5000,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912047/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational cancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.21037/tcr-24-1291","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/2/26 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Centromere protein N (CENPN), a member of the centromere protein family, contributes to ribonucleic assembly, mitosis progression, and chromosome separation. CENPN manifests a close link with the occurrence and progression of several malignant cancers, but there is no pan-cancer study on CENPN, and we aim to ascertain the connection between CENPN and human cancer prognosis and immunotherapy.
Methods: The CENPN function in multiple malignant tumors was comprehensively investigated with data from The Cancer Genome Atlas (TCGA) and integrated Gene Expression Omnibus (GEO) database. We examined the transcriptional level, prognostic effect, diagnostic value, genetic and epigenetic alteration, methylation level, and immunological importance of CENPN. Furthermore, this work provided further confirmation of the phenotypic regulating function of CENPN in breast cancer (BC) cells.
Results: CENPN exhibited significant upregulation in diverse cancer tissues and had different expression patterns across immunological and molecular subgroups in several cancer types. Elevated expression of CENPN may correlate with a worse prognosis. CENPN effectively differentiates most cancers from healthy tissues. Hypomethylate was shown to be CENPN promoter in most cancers. CENPN was shown to be connected with levels of different immune cell infiltration. Kyoto Encyclopedia of Genes and Genomes (KEGG) and the Gene Set Enrichment Analysis (GSEA) analysis suggested that CENPN may mediate neutrophil extranuclear trap formation, cell cycle, and P53 signaling pathways in cancer. In vitro studies showed that the overexpression of CENPN promotes the proliferation, invasion, and migration of BC cells, while concurrently inhibiting their apoptosis.
Conclusions: CENPN may operate as a novel predictive indicator and molecular target for targeted therapy in pan-cancer. Significantly, CENPN contributed to controlling the BC growth and advancement.
期刊介绍:
Translational Cancer Research (Transl Cancer Res TCR; Print ISSN: 2218-676X; Online ISSN 2219-6803; http://tcr.amegroups.com/) is an Open Access, peer-reviewed journal, indexed in Science Citation Index Expanded (SCIE). TCR publishes laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer; results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of cancer patients. The focus of TCR is original, peer-reviewed, science-based research that successfully advances clinical medicine toward the goal of improving patients'' quality of life. The editors and an international advisory group of scientists and clinician-scientists as well as other experts will hold TCR articles to the high-quality standards. We accept Original Articles as well as Review Articles, Editorials and Brief Articles.