NCAPH

Last update 23 Jan 2025

Basic Info

Synonyms

Barren homolog protein 1, BRRN, BRRN1

+ [9]

Introduction

Regulatory subunit of the condensin complex, a complex required for conversion of interphase chromatin into mitotic-like condense chromosomes. The condensin complex probably introduces positive supercoils into relaxed DNA in the presence of type I topoisomerases and converts nicked DNA into positive knotted forms in the presence of type II topoisomerases (PubMed:11136719). Early in neurogenesis, may play an essential role to ensure accurate mitotic chromosome condensation in neuron stem cells, ultimately affecting neuron pool and cortex size (PubMed:27737959).

100 Clinical Results associated with NCAPH

100 Translational Medicine associated with NCAPH

0 Patents (Medical) associated with NCAPH

114

Literatures (Medical) associated with NCAPH

01 Jan 2025·Molecular and Cellular Biochemistry

NCAPH serves as a prognostic factor and promotes the tumor progression in glioma through PI3K/AKT signaling pathway

Article

Author: Yang, Xuejun ; Zhang, Chen ; Wang, Xuya ; Li, Yiming ; Liang, Jianshen ; Fan, Jikang ; Wang, Xisen ; Yu, Shengping ; Jin, Wenzhe ; Li, Tao ; Yun, Debo

AbstractNon-SMC (Structural Maintenance of Chromosomes) condensin I complex subunit H (NCAPH) has been shown to facilitate progression and predict adverse prognostic outcome in many cancer types. However, the function of NCAPH in gliomas is still unclear. Series of experiments were taken to uncover the function of NCAPH in glioma. The expression of NCAPH and potential mechanism regulating progression of glioma was verified by bioinformatics analysis. Lentiviral transfection was used for establishment of loss-of-function and gain-of-function cell lines. CCK-8 assay and Colony-formation assay were used to evaluate proliferation. Transwell assay and Cell wound healing assay were used to assess migration and invasion. Cell cycle and apoptosis were measured by flow cytometry. Protein and RNA were quantified by WB and RT-PCR, respectively. The nude mice model of glioma was used to evaluate the effect of NCAPH in vivo. The expression of NCAPH increased significantly in glioma tissues and correlated with WHO grade, IDH wild-type and non-1p/19q codeletion. Glioma patients with high expression of NCAPH had an undesirable prognosis. Functionally, upregulated NCAPH promotes the malignant hallmarks of glioma cells in vivo and in vitro. NCAPH correlated with DNA damage repair ability of glioma cells and facilitated the proliferation, invasion, and migration of glioma cells by promoting the PI3K/AKT signaling pathway. This study identifies the important pro-tumor role of NCAPH in glioma and suggests that NCAPH is a potential therapeutic target.

01 Nov 2024·Biochemical and Biophysical Research Communications

ZCCHC3 and Efp coordinately contribute to the pathophysiology of triple-negative breast cancer by modulating NCAPH

Article

Author: Inoue, Satoshi ; Fujimoto, Akihiro ; Ikeda, Kazuhiro ; Takeiwa, Toshihiko ; Horie, Kuniko ; Osaki, Akihiko

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with limited targeted therapies and high rates of recurrence. We previously showed that Efp promotes TNBC cell proliferation by regulating cell cycle-related gene expression. Recent studies showed that ZCCHC3 interacts with Efp, promoting Efp signaling in innate immune responses. We here characterize whether ZCCHC3 plays a pathophysiological role in TNBC tumorigenesis. We showed that ZCCHC3 silencing significantly repressed the proliferation of TNBC conventional cultured cells and three-dimensional patient-derived spheroid culture, which we established from a clinical TNBC tissue. RNA-sequencing in TNBC cells defined that "cell division" was a major pathway commonly downregulated by ZCCHC3 and Efp silencing, and NCAPH was a cell division-related gene highly downregulated by ZCCHC3 silencing. In a TNBC cell-derived xenograft model, ZCCHC3-specific siRNA injection successfully reduced in vivo TNBC tumor growth and downregulated NCAPH expression. Overall, our findings demonstrate that ZCCHC3 and Efp coordinately promote TNBC progression by regulating NCAPH expression and that ZCCHC3/Efp/NCAPH pathway can be applied to clinical TNBC management.

01 Sep 2024·Cellular Signalling

The role of NCAPH in cancer treatment

Review

Author: Huang, Manru ; Yu, Haiyang ; Yang, Shenshen ; Pu, Weiling ; Liu, Caiyan ; Zhao, Zixuan ; Han, Xiao ; Zhang, Siqi ; Guo, Bin ; Jin, Jun

Many solid tumors frequently overexpress Non-SMC Condensin I Complex Subunit H (NCAPH), and new studies suggest that NCAPH may be a target gene for clinical cancer therapy. Numerous investigations have shown that a variety of transcription factors, including as MYBL2, FOXP3, GATA3, and OTC1, can stimulate the transcription of NCAPH. Additionally, NCAPH stimulates many oncogenic signaling pathways, such as β-Catenin/PD-L1, PI3K/AKT/SGK3, MEK/ERK, AURKB/AKT/mTOR, PI3K/PDK1/AKT, and Chk1/Chk2. Tumor immune microenvironment modification and tumor growth, apoptosis, metastasis, stemness, and treatment resistance all depend on these signals. NCAPH has the ability to form complexes with other proteins that are involved in glycolysis, DNA damage repair, and chromatin remodeling. This review indicates that NCAPH expression in most malignant tumors is associated with poor prognosis and low recurrence-free survival.

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NCAPH

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