CEP55 antibody
- Known as:
- CEP55 (anti-)
- Catalog number:
- orb100439
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CEP55 antibody
Related genes to: CEP55 antibody
- 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 antibody
Related articles to: CEP55 antibody
- 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 - 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. - Source: PubMed
Publication date: 2026/04/18
Wang JiaxuCao YusongDuan Jianchun - Hepatocellular carcinoma (HCC) often exhibits limited responsiveness to immune checkpoint inhibitors (ICIs), largely due to an immunosuppressive tumor microenvironment (TME). Regulated cell death (RCD) pathways, including ferroptosis, necroptosis, and pyroptosis, possess immunogenic properties that may influence tumor-immune interactions and therapeutic responses. However, the prognostic significance of RCD-related genes and their relationship with immune suppression and anti-PD-1 resistance remain insufficiently understood. Two bulk RNA-seq datasets (GSE181947 and GSE248516) representing immunologically distinct HCC subtypes were analyzed to identify differentially expressed genes (DEGs). These were intersected with curated ferroptosis-, necroptosis-, and pyroptosis-related gene sets, yielding 36 differentially expressed RCD-related genes (DE-RCDRGs). Functional enrichment, protein-protein interaction (STRING and CytoHubba), and survival analyses (Kaplan-Meier Plotter, TCGA-LIHC) were performed to prioritize hub genes. Clinical correlations and epigenetic regulation were assessed using UALCAN. Expression validation was conducted across 24 liver cancer cell lines using Human Protein Atlas (HPA) RNA-seq data. Additionally, deleterious non-synonymous SNPs (nsSNPs) in prioritized genes were structurally characterized using integrative in silico modeling. Ten hub genes were identified, with CEP55, DLGAP5, and EZH2 emerging as key prognostic markers. These genes were significantly overexpressed in tumors, associated with advanced stage and poor differentiation, and showed aberrant DNA methylation. Functional enrichment linked them to oxidative stress response, mitotic regulation, and epigenetic control. Cell-line analysis showed CEP55 and DLGAP5 enrichment in SNU-series models, while EZH2 was highly expressed in HuH-6, Hep3B, and Huh7. Structural analysis further identified deleterious nsSNPs affecting critical functional domains. CEP55, DLGAP5, and EZH2 are identified as RCD-associated biomarkers linked to immune suppression and immunotherapy resistance in HCC. - Source: PubMed
Publication date: 2026/04/15
Azanbayeva DinaraAli AwaisAbdelkarem OmneyaTouir GulnazAlgazina Togzhan - This study investigates the role of centrosomal protein CEP55 in immune evasion by liver cancer cells and evaluates the effects of its knockout using CRISPR-Cas9 technology. CEP55-knockout models were established in human hepatocellular carcinoma cell lines Huh7 and HepG2, and alterations in immune-related molecules, tumor cell behavior, and antitumor immune responses were systematically assessed. CEP55 knockout significantly reduced PD-L1 expression while upregulating MHC class I levels, thereby enhancing tumor immunogenicity. Mechanistically, CEP55 deletion attenuated STAT1 activation, particularly under interferon-γ (IFN-γ) stimulation, suggesting involvement of the IFN-γ-STAT1 signaling axis in CEP55-mediated immune regulation. In parallel, CEP55 knockout markedly decreased intracellular reactive oxygen species (ROS) levels and suppressed the secretion of immunosuppressive cytokines IL-10 and TGF-β, indicating remodeling of the immunosuppressive tumor microenvironment. Functional assays demonstrated that CEP55 deficiency inhibited tumor cell migration and invasion and promoted apoptosis. Importantly, co-culture experiments revealed that CEP55 knockout enhanced T cell effector function, as evidenced by increased secretion of IFN-γ and Granzyme B and restored T cell-mediated cytotoxicity, even in the presence of IFN-γ stimulation. Collectively, these findings indicate that CEP55 promotes liver cancer immune escape and malignant progression through modulation of STAT1-dependent PD-L1/MHC-I expression, oxidative stress, and immunosuppressive signaling. Targeting CEP55 may therefore represent a potential strategy to improve antitumor immune recognition in liver cancer. - Source: PubMed
Publication date: 2026/04/08
Hu ChenweiZhang WeiGe HailongWang YuChao ChenShi XingsongZhou XiaobingWang Chen