ArticleCancer discovery2021
Inhibition of Nuclear Pore Complex Formation Selectively Induces Cancer Cell Death.
Article in Cancer discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 63 citations in OpenAlex.
- Targeted Nanoparticle Delivery CRISPR/Cas9: overcoming biological barriers, enhancing stability, and improving therapeutic precision.International journal of pharmaceutics: X · 2026Review
- Nucleoporins in Cancer: Functional Roles and Therapeutic Opportunities.Cancer discovery · 2026Article
- ADT and activation of HGF and WNT axes in double-null prostate cancer.Nature reviews. Urology · 2026Review
- The molecular basis for nuclear pore destruction by a proximity-inducing molecular glue.Cell chemical biology · 2026Article
- 20 years of taxane therapy in prostate cancer - the past, present and future.Nature reviews. Urology · 2026Review
- Modulation of Nudt21 levels reveals dose-dependent roles of alternative polyadenylation in tissue regeneration.Nature communications · 2026Article
- Nuclear-Cytoplasmic Axis in Cancer: From Protein Mislocalization to Anticancer Drug Resistance.Oncology research · 2026Review
- Dual targeting of AMRC12 andTheranostics · 2026Article
- Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex.Cancer discovery · 2025Article
- Nuclear envelope and chromatin choreography direct cellular differentiation.Nucleus (Austin, Tex.) · 2025Review
- Off-pore Nucleoporin sPOM121 Transcriptionally Propels β-Catenin-driven Tumor Progression and Immune Escape in Prostate Cancer.Cancer discovery · 2025Article
- Histone Deacetylase Inhibitors orchestrate epigenetic signalling and alter the nucleoporins and nuclear envelope in cervical cancer.Translational oncology · 2025Article
- Visualizing developmental dynamics of nuclear morphology and transport machinery in Drosophila.Developmental biology · 2025Article
- Mechanistic models position ceritinib as a nuclear integrity disrupting therapy in pediatric liver tumors.Journal of experimental & clinical cancer research : CR · 2025Article
- Cells prioritize the regulation of cell mass density.Science advances · 2025Article
- Homeostatic regulation of nucleoporins is a central driver of nuclear pore biogenesis.Cell reports · 2025Article
- The Polybrominated Diphenyl Ether Bromoxib Disrupts Nuclear Import and Export by Affecting Nucleoporins of the Nuclear Pore Complex.Marine drugs · 2025Article
- Selinexor as a Therapeutic Target: Advances in Non-small Cell and Small Cell Lung Cancer Treatment Strategies.Recent patents on anti-cancer drug discovery · 2025Review
- Nuclear pore and nucleocytoplasmic transport impairment in oxidative stress-induced neurodegeneration: relevance to molecular mechanisms in Pathogenesis of Parkinson's and other related neurodegenerative diseases.Molecular neurodegeneration · 2024Review
- The Potential of Nuclear Pore Complexes in Cancer Therapy.Molecules (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Nuclear pore complexes (NPC) are the central mediators of nucleocytoplasmic transport. Increasing evidence shows that many cancer cells have increased numbers of NPCs and become addicted to the nuclear transport machinery. How reducing NPC numbers affects the physiology of normal and cancer cells and whether it could be exploited for cancer therapies has not been investigated. We report that inhibition of NPC formation, a process mostly restricted to proliferating cells, causes selective cancer cell death, prevents tumor growth, and induces tumor regression. Although cancer cells die in response to NPC assembly inhibition, normal cells undergo a reversible cell-cycle arrest that allows them to survive. Mechanistically, reducing NPC numbers results in multiple alterations contributing to cancer cell death, including abnormalities in nuclear transport, catastrophic alterations in gene expression, and the selective accumulation of DNA damage. Our findings uncover the NPC formation process as a novel targetable pathway in cancer cells. SIGNIFICANCE: Reducing NPC numbers in cancer cells induces death, prevents tumor growth, and results in tumor regression. Conversely, normal cells undergo a reversible cell-cycle arrest in response to inhibition of NPC assembly. These findings expose the potential of targeting NPC formation in cancer.
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Registered trials
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.