ArticleOncogene2019
Nucleostemin reveals a dichotomous nature of genome maintenance in mammary tumor progression.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed.
- GNL3 SUMOylation is essential for DNA double-strand break repair by homologous recombination.Nature communications · 2026Article
- Nucleostemin promotes RAD51 filament assembly on double-stranded DNA to protect stalled replication forks.Nucleic acids research · 2026Article
- Loss of Drosophila nucleostemin 1 disrupts ribosomal protein homeostasis and rRNA processing to trigger apoptosis via the Xrp1/Irbp18 complex.Cell death discovery · 2026Article
- IMPDH Inhibition Decreases TERT Expression and Synergizes the Cytotoxic Effect of Chemotherapeutic Agents in Glioblastoma Cells.International journal of molecular sciences · 2024Article
- Transcriptional control of a stem cell factor nucleostemin in liver regeneration and aging.PloS one · 2024Article
- Review
- Proteomic Investigation of the Role of Nucleostemin in Nucleophosmin-Mutated OCI-AML 3 Cell Line.International journal of molecular sciences · 2022Article
- Review
- Identification of Binding Proteins for TSC22D1 Family Proteins Using Mass Spectrometry.International journal of molecular sciences · 2021Article
- Quinacrine Induces Nucleolar Stress in Treatment-Refractory Ovarian Cancer Cell Lines.Cancers · 2021Article
- Nucleostemin Modulates Outcomes of Hepatocellular Carcinoma via a Tumor Adaptive Mechanism to Genomic Stress.Molecular cancer research : MCR · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
A defective homologous recombination (HR) repair program increases tumor incidence as well as providing a survival advantage in patients with breast and ovarian cancers. Here we hypothesize that the tumor-promoting side of genome maintenance programs may be contributed by a self-renewal protein, nucleostemin (NS). To address this issue, we established its functional importance in mammary tumor progression in mice and showed that mammary tumor cells become highly susceptible to replicative DNA damage following NS depletion and are protected from hydroxyurea-induced damage by NS overexpression. Breast cancer cells with basal-like characters display more reliance on NS for genome maintenance than those with luminal characters. Mechanistically, NS-deficient cells demonstrate a significantly reduced HR repair activity. TCGA analyses of human breast cancers revealed that NS is co-enriched positively with HR repair proteins and that high NS expression correlates with low HR defects and predicts poor progression-free survival and resistance to knockdown of cell-cycle checkpoint genes in triple-negative/basal-like breast cancers. This work indicates that NS constitutes a tumor-promoting genome maintenance program required for mammary tumor progression.
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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.