Ask about this productRelated 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
- - 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 - Cytokinetic abscission genes are linked to cancers and developmental disorders, but the consequences of disrupted abscission remain under-explored. Previously we showed that in the forebrain of knockout (KO) mouse embryos, a subset of neuroepithelial stem cells (NSCs) fail abscission and become binucleate, and some of those undergo p53-mediated apoptosis. Here we use the KO to investigate how stochastic abscission failures in a polarized epithelium affect the epithelial architecture. We find that NSCs in KO neuroepithelium have preserved epithelial polarity and integrity. However, they have enlarged apical membranes (called apical endfeet), longer primary cilia, and increased biciliation. We then test whether the enlarged apical endfeet arise from filling the space of apoptotic neighbors. Remarkably, blocking apoptosis does not rescue but exacerbates the phenotypes: extra-large apical endfeet have further increased multiciliation, supernumerary centrosomes, and abnormal or multiple nuclei, although epithelial polarity is maintained. These findings elucidate the importance of proper abscission in maintaining polarized epithelial structure, and reveal that p53-mediated apoptosis is a crucial guardian of tissue architecture when cell division defects arise during development and disease. - Source: PubMed
Publication date: 2026/04/08
Lettieri Kaela SMcNeely Katrina CDwyer Noelle D - Engineered extracellular vesicles (EVs) are a class of nonviral delivery vectors for RNA-based vaccines and gene therapies. A specialized form of engineered EVs, known as enveloped protein nanocages (EPNs), has been developed to enhance cargo loading and delivery. When EPNs are equipped with a viral fusogen, such as vesicular stomatitis virus glycoprotein (VSV-G), they have been shown to deliver proteins or RNA efficiently into recipient cells. Comparisons across different EPN types and optimization of their different features have been difficult, as assays for their activity have not been reported for single, active units. As we were interested in optimizing EVs, we first developed a biological titration assay inspired by the methods used for infectious viral particles. With this assay, we optimized EVs using a modular platform, creating EVs composed predominantly of human-derived protein components. This system achieved efficient RNA delivery, with functional titers comparable to those of lentiviral vectors. The optimized chimeric proteins comprising the EV particles integrate domains from human epsin 1, human citramalyl-CoA lyase beta-like protein (CLYBL), and human CEP55. The constructs also include a short 21-amino-acid peptide from a nonhuman source for RNA packaging, resulting in an EV-based RNA delivery system with reduced immunogenicity compared with EPNs and retroviral virus-like particles (VLPs). - Source: PubMed
Publication date: 2026/04/07
Ma XiangZhao Sophia RCepko Constance L