Ask about this productRelated genes to: CEP55 Blocking Peptide
- Gene:
- CEP55 NIH gene
- Name:
- centrosomal protein 55
- Previous symbol:
- C10orf3
- Synonyms:
- FLJ10540, CT111
- Chromosome:
- 10q23.33
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-24
- Date modifiied:
- 2019-03-14
Related products to: CEP55 Blocking Peptide
Related articles to: CEP55 Blocking Peptide
- Myelodysplastic neoplasms (MDS) are clonal hematopoietic disorders defined by ineffective hematopoiesis, cytopenias, and variable risk of progression to acute myeloid leukemia. Although genomic and epigenomic studies have provided insight into disease pathogenesis, reliable biomarkers for diagnosis and prognosis remain limited. Proteomics offers an important advantage because it reflects the functional protein state and captures post-translational modifications, making it highly relevant for risk assessment and therapy guidance. Recent studies have identified several groups of candidate biomarkers. Kinases and signal transduction proteins such as CAMK1D, PRKCZ, KIT, MAST4, PAK6, PTK7, and NTRK1 are dysregulated in MDS and associated with poor outcomes, immune evasion, and aberrant stem cell signaling. Oncofetal proteins like IGF2BP3 and signaling regulators such as RBP4 further highlight proteomic signatures linked to chemoresistance and subtype specificity. In the transplant setting, immune regulators including CSK, FGR, CRTAM, GP1BA, UBE2N, and STAT1 may serve as predictors of graft rejection and relapse. Cytoskeletal and extracellular matrix proteins such as CEP55, Talin-1, Kindlin-3, Vinculin, THBS1, LRG1, SPARC, SAA1, Clusterin, and PRDM16 underscore the role of bone marrow microenvironmental remodeling and adhesion defects in disease progression. Finally, metabolic enzymes such as LDHA reflect altered energy metabolism and correlate with more aggressive disease biology. Collectively, these proteomic candidates illustrate the complex interplay of signaling, immune regulation, bone microenvironment, and metabolism in MDS. Their validation in clinical cohorts could enable early detection, refined risk stratification, and new therapeutic avenues, positioning proteomics as a central tool in the future management of MDS. - Source: PubMed
Novak RuđerMandac Smoljanović IngaGrgurević Lovorka - Lung adenocarcinoma (LUAD) is the most lethal subtype of lung cancer, and its occurrence and progression are closely correlated with immune escape. CEP55 is upregulated in a variety of malignancies and participates in tumor progression, yet its specific role in the immune regulation of LUAD remains poorly defined. Due to the unclear mechanism of immune escape, the therapeutic efficacy of immunotherapy for LUAD is still unsatisfactory. Therefore, it is essential to further elucidate the underlying molecular mechanisms and identify novel therapeutic targets. This study aims to explore the biological function of CEP55 in LUAD immune escape, as well as to clarify its upstream regulatory mechanism and downstream signaling pathways. CEP55 expression in LUAD tissues was assessed utilizing data from TCGA-LUAD and validated in cells. Bioinformatics approaches were employed to explore CEP55-enriched signaling pathways and their link to CD8⁺ T cell infiltration. A CD8⁺ T-tumor cell co-cultured model was established, and LDH release, ELISA, and CFSE staining were utilized to assess CD8⁺ T cell cytotoxicity and proliferation. To uncover the role of CEP55 in LUAD cell behavior, we employed CCK-8, EdU labeling, Transwell assays, and flow cytometry to systematically evaluate its effects on proliferation, migration, invasion, and apoptosis. Western blotting was performed to measure key signaling pathway proteins expression level. Potential upstream regulators of CEP55 mA modification were identified through database mining, followed by validation using RIP, MeRIP-qPCR, and WB. CEP55 was highly expressed in LUAD and inversely associated with CD8⁺ T cell infiltration. Knockdown of CEP55 in LUAD enhanced tumor-killing activity of CD8⁺ T cells in a co-culture system and significantly suppressed LUAD cell proliferation, migration, invasion, and anti-apoptotic capacity. CEP55 was positively correlated with WTAP in LUAD. WTAP stabilized CEP55 mRNA expression via mA modification, while CEP55 activated the PI3K/AKT/mTOR pathway, upregulating PD-L1. This led to CD8⁺ T cell exhaustion and promoted tumor immune evasion. This study reveals a critical mechanism whereby WTAP upregulates CEP55 expression via m⁶A modification, thereby activating the PI3K/AKT/mTOR signaling pathway, inhibiting the anti-tumor activity of CD8⁺ T cells, and ultimately facilitating LUAD progression. These findings indicate that CEP55 serves as a promising therapeutic target for LUAD immunotherapy, providing novel theoretical evidence to improve the efficacy of immune treatment. - Source: PubMed
Publication date: 2026/06/16
Yang TianyuChen TaoYang Ran - Ovarian cancer (OVCA) remains the most lethal gynecologic malignancy, with poor prognosis largely due to late-stage diagnosis and therapy resistance. Pyroptosis, a pro-inflammatory form of programmed cell death, has recently emerged as a regulator of tumor progression and immune regulation. This study aimed to systematically profile pyroptosis-related genes and identify robust biomarkers for OVCA. Microarray data from the GSE54388 dataset were analyzed to characterize pyroptosis-related gene expression. Immune cell infiltration was assessed using xCell, and pathway enrichment was performed via Gene Set Enrichment Analysis (GSEA). Weighted Gene Co-expression Network Analysis (WGCNA) identified hub genes, followed by Gene Ontology (GO) and Reactome enrichment. Machine learning algorithms (Support Vector Machine, XGBoost, and Generalized Linear Model) were employed for feature selection and biomarker identification. Validation was conducted across independent bulk and scRNA-seq datasets, with GEPIA2 used to compare OVCA and normal samples and KMplot for survival analysis. OVCA samples showed significantly reduced infiltration of CD4 and CD8 T cells, mast cells, monocytes, neutrophils, and immature dendritic cells compared to normal samples. GSEA revealed enrichment of cell cycle-related pathways, implicating pyroptosis-related genes as key regulators of mitotic progression. From 1097 differentially expressed genes, 22 pyroptosis-related DEGs (PYRDEGs) were identified, with nine hub genes (CASP1, CEP55, CHMP4C, HTRA1, IL18, MELK, PKM, PTX3, TNFSF13B) strongly associated with OVCA. Functional enrichment linked these genes to cytokinesis, inflammasome activity, and immune signaling. Machine learning consistently identified CEP55 as the core biomarker, demonstrating high diagnostic accuracy (AUC up to 0.972) and significant upregulation in OVCA samples. Correlation analysis linked CEP55 expression to altered immune cell populations, including positive associations with Th1 and class-switched memory B-cells and negative associations with iDCs, Tregs, and M2 macrophages. CEP55 was highly expressed across bulk and scRNA-seq datasets (cancer epithelial and CD8+ TEMRA cells) and negatively correlated with overall survival (OS) and progression-free survival (PFS). Pyroptosis-related genes play pivotal roles in OVCA pathogenesis. CEP55 emerges as a promising biomarker for early detection and a potential therapeutic target, bridging cell cycle regulation with immune modulation. - Source: PubMed
Publication date: 2026/05/21
Arya RakeshBiswas Viplov KumarShakya HemlataKim Jong-Joo - Liver hepatocellular carcinoma (LIHC) is an aggressive cancer associated with chronic liver disease, necessitating better biomarkers and therapies. Manganese, an essential trace element, regulates tumor development. Data from TCGA and GEO databases were analyzed to identify manganese metabolism-related genes (MMRGs). LIHC samples were classified into subtypes via consensus clustering. A prognostic model was developed using LASSO and multivariate Cox regression, then validated using ROC and survival analysis. Immune infiltration was assessed via ssGSEA and CIBERSORT, and cell communication was analyzed with single-cell data (GSE149614). Tumor Mutational Burden (TMB), drug sensitivity, and a nomogram were also evaluated. Two manganese metabolism-related subtypes were identified, with Cluster 1 showing better survival. A two-gene model (CEP55 and SPP1) reliably predicted poor prognosis in high-risk groups. The high-risk group exhibited distinct immune profiles, including increased immune infiltration, elevated checkpoint expression, and higher TIDE scores. Single-cell analysis revealed altered T cell communication. This study established manganese metabolism-related subtypes and a prognostic model for LIHC, providing insights into immunoregulation and cell communication to guide precision diagnosis and immunotherapy. - Source: PubMed
Publication date: 2026/04/29
Liu ChunhuiZhang WenqiLuo WenziZhang CaifengZhang BoZhang GuozhiWang XiaotaoChen JianliZhou Han - BACKGROUND: Non-small cell lung cancer (NSCLC) is one of the primary contributors to global cancer mortality. Elevated expression of centrosomal protein 55 (CEP55) is frequently observed in NSCLC and is closely linked to tumorigenesis and disease progression. However, the prognostic value of CEP55 in NSCLC has not been fully established. The current meta-analysis assessed how increased CEP55 expression may influence prognosis in patients diagnosed with NSCLC. METHODS: Eligible studies were retrieved via a systematic search across major biomedical databases. Additionally, validation cohorts were retrieved from the Gene Expression Omnibus (GEO) database. To quantify the prognostic relevance of CEP55, hazard ratios (HRs) and 95% confidence intervals (CIs) were synthesized from eligible studies. The Newcastle-Ottawa Scale was leveraged to assess the methodological quality of the included studies. This review was registered with PROSPERO (CRD420251006676). RESULTS: A total of 18 independent study cohorts (6 literature-derived and 12 database-derived) involving 4,829 patients were included. The meta-analysis revealed that elevated CEP55 expression was significantly associated with poorer overall survival (OS) in NSCLC patients [HR = 1.22, 95% CI: 1.13–1.32]. Subgroup analysis by histological subtype showed that CEP55 serves as an independent predictor of poor OS in lung adenocarcinoma (LUAD) [HR = 1.28, 95% CI: 1.20–1.37], whereas its prognostic utility in lung squamous cell carcinoma (LUSC) was not statistically significant [HR = 0.98, 95% CI: 0.90–1.06]. Multivariate analysis further confirmed CEP55 as an independent risk factor for LUAD, with its prognostic impact being particularly evident in early-stage disease characteristics—including Stage I, limited tumor infiltration (T1–T2), and the absence of distant metastasis (M0)—as well as in patients with negative surgical margins or those who had not received chemotherapy. CONCLUSION: CEP55 may act as a potential indicator for predicting disease progression and survival outcomes in NSCLC, particularly in LUAD. Further investigation into the underlying mechanisms of CEP55 is necessary. - Source: PubMed
Publication date: 2026/04/18
Wang JiaxuCao YusongDuan Jianchun