ArticleCell cycle (Georgetown, Tex.)2022
NCAPH promotes cell proliferation and inhibits cell apoptosis of bladder cancer cells through MEK/ERK signaling pathway.
Article in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- MiR-1976 affects lung squamous cell carcinoma development by targeting NCAPH.Journal of applied genetics · 2026Article
- Non-structural maintenance of chromosome condensin I complex subunit H knockdown suppresses malignant progression of esophageal squamous cell carcinoma via the Wnt/β-catenin signaling pathway.Journal of gastrointestinal oncology · 2026Article
- Comprehensive bioinformatics analysis of NCAPH expression and its clinical importance in endometrial cancer.Oncology letters · 2026Article
- Non-SMC condensin I complex subunit H promotes cell proliferation and inhibits cell apoptosis of clear cell renal cell carcinoma by activating the PI3K/AKT pathway.Translational andrology and urology · 2025Article
- The MDM2-p53 axis regulates norrin/frizzled4 signaling and blood-CNS barrier function.Science signaling · 2025Article
- NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathway.Journal of ovarian research · 2025Article
- NCAPH as a potential prognostic signaling biomarker regulating low-grade glioma cell proliferation, migration, invasion, immune microenvironment, and drug sensitivity.Journal of Cancer · 2025Article
- NCAPH serves as a prognostic factor and promotes the tumor progression in glioma through PI3K/AKT signaling pathway.Molecular and cellular biochemistry · 2025Article
- NCAPH Promotes the Proliferation of Prostate Cancer Cells Via Modulating the E2F1 Mediated PI3K/AKT/mTOR Axis.International journal of medical sciences · 2025Article
- Circ_0001047 inhibits prostate cancer progression and enhances abiraterone sensitivity via miR-122-5p/FKBP5/PHLPP1/AKT axis in vitro.Discover oncology · 2024Article
- DOCK1 regulates the malignant biological behavior of endometrial cancer through c-Raf/ERK pathway.BMC cancer · 2024Article
- NCAPH drives breast cancer progression and identifies a gene signature that predicts luminal a tumour recurrence.Clinical and translational medicine · 2024Article
- Article
- NCAPH Drives Breast Cancer Progression and Identifies a Gene Signature that Predicts Luminal A Tumor Recurrence.Research square · 2023Article
- Non-SMC condensin I complex subunit H participates in anti-programmed cell death-1 resistance of clear cell renal cell carcinomas.Cell proliferation · 2023Article
- The TT Genotype of theCells · 2023Article
- Identification of key genes associated with cancer stem cell characteristics in Wilms' tumor based on bioinformatics analysis.Annals of translational medicine · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder cancer (BC) is one of the most common cancers world-wide with a poor prognosis. Non-SMC (Structural Maintenance of Chromosomes)-condensin I complex subunit H (NCAPH) is a regulatory subunit of the condensin I complex and plays an important role in tumorigenesis and progression in several types of cancers. However, the role of NCAPH in BC remains unknown. In this study, we tried to reveal the biological functions of NCAPH in BC. We detected the expressions of NCAPH in BC and adjacent tissues, and BC cells lines. Subsequently, the gain- and loss-of-function experiments were performed to determine the effects of NCAPH on BC cell proliferation, apoptosis, and activation of the MEK/ERK signaling pathway in vitro. Moreover, we used BALB/c nude mice and established a xenograft model to investigate whether silence NCAPH using shRNA targeting NCAPH (shNCAPH) can inhibit BC tumor growth in vivo. The results showed NCAPH was overexpressed in BC tissues compared to adjacent tissues and highly expressed in BC cell lines. Additionally, overexpression of NCAPH promoted cell proliferation and inhibited apoptosis in SW780 cells. Conversely, knockdown of NCAPH reduced cell proliferation and enhanced apoptosis in UMUC3 cells. Furthermore, we found that the NCAPH activated the MEK/ERK signaling pathway in BC cells. MEK1/2 inhibitor U0126 blocked the increase of cell proliferation regulated by NCAPH overexpression. Knockdown of NCAPH significantly inhibited tumor growth in mice. Our results suggest that NCAPH might play an important role in BC progression and provide the potential marker in the diagnosis of BC.
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