ArticleThe Journal of clinical investigation2016
Nuclear pore protein NUP88 activates anaphase-promoting complex to promote aneuploidy.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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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
27 citing papers in PubMed, 39 citations in OpenAlex.
- The nuclear pore complex as a spatial organizing hub for high-risk DNA lesions.Nucleus (Austin, Tex.) · 2026Review
- Nucleoporins in Cancer: Functional Roles and Therapeutic Opportunities.Cancer discovery · 2026Article
- Cartilage Oligomeric Matrix Protein Promotes Radiation Resistance in Non-Small Cell Lung Cancer In Vitro.International journal of molecular sciences · 2025Article
- Targeting CLK2 and serine/arginine-rich splicing factors inhibits multiple myeloma through downregulating RAE1 by nonsense-mediated mRNA decay mechanism.Cancer science · 2025Article
- Interdependence between Nuclear Pore Gatekeepers and Genome Caretakers: Cues from Genome Instability Syndromes.International journal of molecular sciences · 2024Review
- Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024Review
- Nuclear envelope budding and its cellular functions.Nucleus (Austin, Tex.) · 2023Article
- Nuclear transport proteins: structure, function, and disease relevance.Signal transduction and targeted therapy · 2023Review
- GermlineInternational journal of molecular sciences · 2023Article
- Overexpressed Nup88 stabilized through interaction with Nup62 promotes NF-κB dependent pathways in cancer.Frontiers in oncology · 2023Article
- Glutamine synthetase licenses APC/C-mediated mitotic progression to drive cell growth.Nature metabolism · 2022Article
- Overexpression of the nucleoporin Nup88 stimulates migration and invasion of HeLa cells.Histochemistry and cell biology · 2021Article
- Ribonucleic Acid Export 1 Is a Kinetochore-Associated Protein That Participates in Chromosome Alignment in Mouse Oocytes.International journal of molecular sciences · 2021Article
- Glycolysis Changes the Microenvironment and Therapeutic Response Under the Driver of Gene Mutation in Esophageal Adenocarcinoma.Frontiers in genetics · 2021Article
- Long non-coding RNA MILNR1 retards colorectal cancer growth by inhibiting c-Myc.Cancer communications (London, England) · 2020Article
- Nesprin-1 impact on tumorigenic cell phenotypes.Molecular biology reports · 2020Article
- BubR1 allelic effects drive phenotypic heterogeneity in mosaic-variegated aneuploidy progeria syndrome.The Journal of clinical investigation · 2020Article
- Oncogenic potential of nucleoporins in non-hematological cancers: recent update beyond chromosome translocation and gene fusion.Journal of cancer research and clinical oncology · 2019Review
- Biallelic mutations in nucleoporin NUP88 cause lethal fetal akinesia deformation sequence.PLoS genetics · 2018Article
- Moonlighting nuclear pore proteins: tissue-specific nucleoporin function in health and disease.Histochemistry and cell biology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The nuclear pore complex protein NUP88 is frequently elevated in aggressive human cancers and correlates with reduced patient survival; however, it is unclear whether and how NUP88 overexpression drives tumorigenesis. Here, we show that mice overexpressing NUP88 are cancer prone and form intestinal tumors. To determine whether overexpression of NUP88 drives tumorigenesis, we engineered transgenic mice with doxycycline-inducible expression of Nup88. Surprisingly, NUP88 overexpression did not alter global nuclear transport, but was a potent inducer of aneuploidy and chromosomal instability. We determined that NUP88 and the nuclear transport factors NUP98 and RAE1 comprise a regulatory network that inhibits premitotic activity of the anaphase-promoting complex/cyclosome (APC/C). When overexpressed, NUP88 sequesters NUP98-RAE1 away from APC/CCDH1, triggering proteolysis of polo-like kinase 1 (PLK1), a tumor suppressor and multitasking mitotic kinase. Premitotic destruction of PLK1 disrupts centrosome separation, causing mitotic spindle asymmetry, merotelic microtubule-kinetochore attachments, lagging chromosomes, and aneuploidy. These effects were replicated by PLK1 insufficiency, indicating that PLK1 is responsible for the mitotic defects associated with NUP88 overexpression. These findings demonstrate that the NUP88-NUP98-RAE1-APC/CCDH1 axis contributes to aneuploidy and suggest that it may be deregulated in the initiating stages of a broad spectrum of human cancers.
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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.