ArticleOncology letters2022
Non-SMC condensin I complex subunit H promotes the malignant progression and cisplatin resistance of breast cancer MCF-7 cells.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Comprehensive bioinformatics analysis of NCAPH expression and its clinical importance in endometrial cancer.Oncology letters · 2026Article
- NCAPD2 promotes the progression of lung adenocarcinoma through an AKT/MDM2/E2F1 positive feedback loop.Cancer biology & therapy · 2025Article
- NCAPH Promotes the Proliferation of Prostate Cancer Cells Via Modulating the E2F1 Mediated PI3K/AKT/mTOR Axis.International journal of medical sciences · 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
- Integrated bioinformatics combined with machine learning to analyze shared biomarkers and pathways in psoriasis and cervical squamous cell carcinoma.Frontiers in immunology · 2024Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is one of the most frequently diagnosed types of cancer worldwide. The present study aimed to investigate the role and underlying regulatory mechanism of non-structural maintenance of chromosome condensin I complex subunit H (NCAPH) in the malignant progression and cisplatin (DDP) resistance of breast cancer cells. Therefore, the mRNA and protein expression levels of NCAPH were first determined in breast cancer cells via reverse transcription-quantitative PCR and western blotting. Furthermore, following transfection of NCAPH interference plasmids, the effect of NCAPH knockdown on cell proliferation, migration, invasion were also assessed using CCK-8, wound healing and Transwell assays. Apoptosis was evaluated using TUNEL assay, and western blotting was performed in breast cancer cells and DDP-resistant breast cancer cells. The association between NCAPH and its downstream target, aurora kinase B (AURKB), was verified using bioinformatic analysis and the co-immunoprecipitation assay. Furthermore, the effect of AURKB overexpression on the aforementioned processes and the Akt/mTOR signaling pathway were also assessed. The results demonstrated that NCAPH mRNA and protein expression levels were significantly upregulated in breast cancer cells, whereas NCAPH knockdown significantly attenuated the proliferation, migration and invasion of breast cancer cells. NCAPH silencing also exacerbated the apoptosis of DDP-resistant breast cancer cells. AURKB mRNA and protein expression levels were also significantly upregulated in MCF-7 cells, whereas its overexpression significantly reversed the effects of NCAPH knockdown on breast cancer cells and the Akt/mTOR signaling pathway. Overall, NCAPH knockdown significantly downregulated AURKB mRNA and protein expression levels to block the Akt/mTOR signaling pathway and inhibited breast cancer cell proliferation, migration, invasion, and aggravate DDP-resistant breast cancer cell apoptosis, indicating that NCAPH may serve as a promising therapeutic target for breast cancer.
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