ArticleCell death & disease2017
NCAPH plays important roles in human colon cancer.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 90 citations in OpenAlex.
- 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
- 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
- NCAPH serves as a prognostic factor and promotes the tumor progression in glioma through PI3K/AKT signaling pathway.Molecular and cellular biochemistry · 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 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
- NCAPH, ubiquitinated by TRIM21, promotes cell proliferation by inhibiting autophagy of cervical cancer through AKT/mTOR dependent signaling.Cell death & disease · 2024Article
- MiR-1976/NCAPH/P65 axis inhibits the malignant phenotypes of lung adenocarcinoma.Scientific reports · 2024Article
- Knockdown of NCAPD3 inhibits the tumorigenesis of non-small cell lung cancer by regulation of the PI3K/Akt 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
- Role and mechanism ofFrontiers in pharmacology · 2024Article
- GPR168 functions as a tumor suppressor in mouse melanoma by restraining Akt signaling pathway.PloS one · 2024Article
- 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
- Identification of Prognostic Biomarkers for Suppressing Tumorigenesis and Metastasis of Hepatocellular Carcinoma through Transcriptome Analysis.Diagnostics (Basel, Switzerland) · 2023Article
- Article
- NCAPH is a prognostic biomarker and associated with immune infiltrates in lung adenocarcinoma.Scientific reports · 2022Article
- Identification of hub genes and biological pathways in glioma via integrated bioinformatics analysis.The Journal of international medical research · 2022Article
- MrgprF acts as a tumor suppressor in cutaneous melanoma by restraining PI3K/Akt signaling.Signal transduction and targeted therapy · 2022Article
- NCAPH promotes cell proliferation and inhibits cell apoptosis of bladder cancer cells through MEK/ERK signaling pathway.Cell cycle (Georgetown, Tex.) · 2022Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colon cancer (CC) is one of the major malignancies worldwide, whose pathogenesis is complex and requires the accumulated alteration of multiple genes and signaling pathways. Condensins are multi-protein complexes that play pivotal roles in chromosome assembly and segregation during mitosis, meiosis and even tumorigenesis. Using tissue microarrays by immunohistochemistry and hematoxylin-eosin staining, we found that non-SMC condensin I complex subunit H (NCAPH) in colon cancerous tissues was higher than that in all corresponding adjacent non-cancerous tissues. We then characterized the exact function of the NCAPH in CC. We provided evidences showing that NCAPH is highly expressed in colorectal cancer cell lines comparing with normal human colonic epithelial cells, and identified many NCAPH mutations in CC patients. We found that depletion of NCAPH inhibits CC cell proliferation, migration in vitro and xenograft tumor formation in vivo. Furthermore, NCAPH knockdown promotes cell apoptosis and cell cycle arrest at G2/M phase. Interestingly, the NCAPH high expression in tumor tissues of colon patients had a significantly better prognosis and survival rate than low-expression patients, suggesting that NCAPH high expression promotes colonic cancerous cell proliferation; on the other hand, it may also sensitize these cells responding to chemo- or radio-therapies. Collectively, these findings reveal an important role of NCAPH in CC, indicating that NCAPH could be used as a new therapeutic target in future.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.