Ask about this productRelated genes to: NCAPH Blocking Peptide
- Gene:
- NCAPH NIH gene
- Name:
- non-SMC condensin I complex subunit H
- Previous symbol:
- BRRN1
- Synonyms:
- CAP-H, hCAP-H
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-11
- Date modifiied:
- 2015-11-12
Related products to: NCAPH Blocking Peptide
Related articles to: NCAPH Blocking Peptide
- Brain metastasis (BM) represents a significant clinical challenge in advanced breast cancer, yet the molecular mechanisms driving breast cancer brain metastasis (BCBM) remain incompletely characterized. This study aims to identify key molecular pathways and hub genes specifically associated with BCBM through comprehensive bioinformatic analyses. Gene Set Enrichment Analysis (GSEA), differential gene expression analysis, and weighted gene co-expression network analysis (WGCNA) were performed using two independent GEO datasets (GSE191230 and GSE43837). Protein-protein interaction (PPI) networks were constructed to visualize functional interconnections among dysregulated genes. Survival analyses were conducted using the Kaplan-Meier Plotter database to evaluate the prognostic significance of identified hub genes. GSEA revealed significant upregulation of metabolic pathways (mTORC1 signaling, glycolysis, oxidative phosphorylation) and downregulation of immune-related pathways in BCBM compared to primary tumors. Integrative analysis identified 34 consistently dysregulated genes across datasets, from which 12 hub genes were validated. Among these, RRM2, CDCA8, CCNB1, LMNB2, FANCI, NCAPH, YWHAZ, and ESPL1 demonstrated brain-specific over-expression compared to other metastatic sites. Functional enrichment analysis highlighted cell cycle dysregulation as a critical mechanism in BCBM, and all hub genes showed significant association with poor prognosis in breast cancer patients. This study identifies a unique molecular profile of BCBM characterized by cell cycle dysregulation, metabolic reprogramming, and immune microenvironment alterations. The brain-specific expression patterns of these hub genes represent potential biomarkers for BCBM risk assessment and novel therapeutic targets, providing a basis for precision medicine development. - Source: PubMed
Publication date: 2026/04/13
Ting Wei-YiLu Yueh-HsunLin Che-Ming - Chromatin architecture is increasingly recognized as a fundamental regulatory layer that enables cancer cells to integrate genetic instability, transcriptional plasticity, metabolic adaptation, and immune escape. NCAPH, a non-SMC regulatory subunit of the condensin I complex, has long been regarded as a mitosis-associated chromosome condensation factor. However, accumulating evidence across multiple cancer types reveals that NCAPH plays far broader roles in malignant progression and therapeutic resistance. In this review, we synthesize recent advances to position NCAPH as an onco-structural hub that links higher-order chromatin organization to genome stability, metabolic reprogramming, immune evasion, and therapy resistance. We first summarize the biological features of NCAPH within the condensin I system and highlight its dosage-sensitive effects on chromatin mechanics and DNA damage response. We then integrate pan-cancer evidence demonstrating that NCAPH overexpression is associated with aggressive clinicopathological features, poor prognosis, immune suppression, and resistance to chemotherapy, targeted therapy, radiotherapy, and immune checkpoint blockade. Mechanistically, NCAPH-mediated chromatin remodeling supports glycolytic and anabolic metabolism, stabilizes immune checkpoint signaling such as PD-L1, sustains stemness and epithelial-mesenchymal plasticity, and enables adaptive tolerance to genotoxic and immunological stress. Finally, we discuss the translational implications of targeting the NCAPH axis, including its potential as a biomarker for patient stratification and as a therapeutic vulnerability for rational combination strategies. By integrating structural genome biology with cancer metabolism and tumor immunology, this review provides a unifying framework for understanding how chromatin architectural regulators drive malignant fitness and highlights key challenges and future directions for exploiting NCAPH-mediated chromatin adaptability in precision oncology. - Source: PubMed
Publication date: 2026/03/11
Song ZhaopengXia YitongZhang GuifengWang ZhengYang JingkunFan Wenyong - Head and neck squamous cell carcinoma (HNSCC) is an epithelial carcinoma characterized by its distinct geographical distribution, exhibiting a higher prevalence in Southeast Asia. Despite the approval of immune checkpoint blockade (ICB) therapy for treating advanced recurrent HNSCC, the extent of patient benefit remains limited. Elucidating the molecular regulatory mechanisms of immunosuppressive tumor microenvironment in HNSCC is crucial for improving current treatment status and patient outcomes. Our findings show that knockdown of NCAPH suppresses cell proliferation, migration, and xenograft tumor growth, while enhancing radiotherapy-induced cellular apoptosis. Importantly, we found that NCAPH binds to PD-L1 and disrupts its degradation, competing with HIP1R (Huntingtin-interacting protein 1-related) and leading to the stabilization of PD-L1 protein, which contributes to the formation of immunosuppressive tumor microenvironment. To inhibit the interaction between NCAPH and PD-L1, we created a peptide known as NPIDP (NCAPH and PD-L1 Interaction Disrupting Peptide) that effectively disrupts the interaction between NCAPH and PD-L1. Furthermore, topotecan, a well-characterized topoisomerase I inhibitor, was identified to bind NCAPH and promote its proteasomal degradation. Notably, we demonstrated that NPIDP and topotecan suppress tumor immune evasion both in vitro and in vivo. In summary, our findings reveal the critical role of NCAPH in regulating tumor immune surveillance, suggesting that NCAPH could serve as a potential biomarker and therapeutic target for HNSCC in the future. - Source: PubMed
Publication date: 2025/12/11
Liu BaiyangXiang XudongCheng YanFei JiminWu MenggeQu LaihaoZhao XianChen XingLi YaoDu JiaMu DengcaiZhai HaoqingShen QiushuoChen YongbinYang Cuiping - NCAPH is mainly involved in the transformation of nuclear chromatin in the intercellular phase into a highly heliform nuclear chromosome, encoded by a gene on chromosome 2q11.2. Studies have found that NCAPH, as an oncogene, plays important roles in the occurrence and development of several cancers, significantly affecting the survival and prognosis of patients. However, the role of NCAPH in low-grade glioma (LGG) has been largely unexplored. Here, we conduct a comprehensive analysis of NCAPH expression, abundance of cell subsets in single-cell cohorts, prognosis, co-localization, epigenetic alterations, functional enrichment, tumor immune-related features, immunotherapy response, drug sensitivity, and molecular docking in LGG. Our findings suggest that NCAPH is significantly overexpressed in LGG and is strongly relevant to poor prognosis, and that NCAPH plays important roles in reshaping the tumor microenvironment, which may promote immune tolerance of LGG and thus become a potential immunotherapeutic target. The sensitivity of LGG patients with high NCAPH expression to chemotherapy agents such as temozolomide also suggests the potential therapeutic effect of chemotherapy combined with immunotherapy. Furthermore, NCAPH was positively correlated with cell cycle, proliferation, DNA damage and repair, EMT, invasion, and apoptosis, while negatively associated with inflammation, quiescence and angiogenesis. Together, this study provides a comprehensive understanding of the role of NCAPH in LGG and suggests that NCAPH may be a potential prognostic biomarker for LGG patients, with potential for drug development and immunotherapy. - Source: PubMed
Publication date: 2025/09/27
Dai LiruiJiang ShuZhou Peizhi - This study evaluated the prognostic role of E2F transcription factor 2 (E2F2) in serous ovarian cancers (SOCs) and explored its biological functions, immune cell infiltration links, and therapeutic implications. - Source: PubMed
Publication date: 2025/09/23
Jiang FengyinFei HeYang LinaChen RujunZhang Liwen