ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Disruption of ARID1B Recruitment to the Nuclear Pore Complex as a New Anticancer Therapeutic Strategy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed.
- Proteomic characterization of SMARCA-deficient esophageal adenocarcinoma reveals complement evasion and DNA repair-associated prognostic subgroups.British journal of cancer · 2026Article
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- Long term survival of patients with alpha-fetoprotein-positive hepatoid adenocarcinoma of the gallbladder: a case report and literature review.Frontiers in oncology · 2026Article
- Disruption of ARID1B Recruitment to the Nuclear Pore Complex as a New Anticancer Therapeutic Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC), a highly aggressive subtype, currently lacks potent targeted therapies. ARID1B, a key SWI/SNF chromatin remodeling complex subunit, is linked to high-grade malignancies and poor prognosis, making it a potential biomarker and therapeutic target. However, its function and regulation remain unclear. Here, it is found that uncontrolled accumulation of ARID1B and its dysregulated nuclear import promoted oncogenesis and drug resistance. ARID1B negatively regulates ARID1A, impairing SWI/SNF-mediated tumor suppression and enhancing tumor survival. Using protein complex purification and mass spectrometry, the KPNA2-KPNB1-RANBP2 protein cascade is identified as critical for facilitating ARID1B nuclear import. Replacing R1518, H1519, and D1522 residues on ARID1B with T1518, G1519, and G1522 attenuates the ARID1B-KPNA2/KPNB1 interaction, preventing recruitment of ARID1B to the nuclear pore complex (NPC). Pharmacologically inhibiting KPNB1 suppressed ARID1B translocation, limiting its nuclear levels. In TNBC mouse models, ARID1B knockout (KO) significantly reduces tumor growth and enhances PARP inhibitor efficacy. Collectively, these findings uncover an undocumented mechanism for ARID1B nuclear translocation and reveal that blockade of ARID1B nuclear translocation can be a new therapeutic strategy for TNBC.
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Registered trials
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