ArticleScientific reports2025
The inner nuclear membrane protein, Banf1, has an essential role in triple negative breast cancer cell proliferation and survival.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- BANF1 as a potential prognostic biomarker associated with tumor-intrinsic programs and a complex immune landscape in lung adenocarcinoma.Discover oncology · 2026Article
- Barrier-to-Autointegration Factor 1: a key regulator of nuclear envelope integrity, genome stability, and disease progression.Frontiers in immunology · 2026Review
- BANF1 knockdown impedes thyroid cancer development and boosts CD8American journal of cancer research · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple negative breast cancers (TNBCs) are a heterogenous subcategory of breast cancers which have significantly worse survival outcomes compared to other breast cancer subtypes. However, limited advances have been made towards a targeted TNBC therapeutic and traditional chemotherapies remain the frontline therapy. Therefore, this study aimed to examine the therapeutic potential of a novel TNBC target, Barrier-to-Autointegration Factor 1 (Banf1), including determining Banf1 expression and cellular localisation in non-malignant breast cells and a panel of TNBC cell lines. Bioinformatic analysis of patient samples demonstrated that Banf1 is overexpressed in all breast cancer stages and subtypes. Banf1 depletion inhibited proliferation and induced mitotic arrest in TNBC cells via loss of nuclear envelope integrity and aberrant nuclear morphology, inducing TNBC tumour cell-specific cell death. These findings highlight the significant overexpression and functional involvement of Banf1 in TNBC progression and suggests that it may have potential as a novel anti-cancer target, supporting further investigation.
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