ArticleOncogene2017
p53 deficiency induces cancer stem cell pool expansion in a mouse model of triple-negative breast tumors.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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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
16 citing papers in PubMed, 23 citations in OpenAlex.
- TSPYL5-driven G3BP1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating RanBP2-mediated p53 sumoylation and nuclear export in neuroblastoma.Cell death & disease · 2025Article
- A Review of Radiation-Induced Alterations of Multi-Omic Profiles, Radiation Injury Biomarkers, and Countermeasures.Radiation research · 2023Review
- Smad4 and p53 synergize in suppressing autochthonous intestinal cancer.Cancer medicine · 2022Article
- Orthotopic Transplantation of Mouse Mammary Epithelial Cells.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Identification of potential therapeutic target of naringenin in breast cancer stem cells inhibition by bioinformatics andSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021Article
- BCL11B suppresses tumor progression and stem cell traits in hepatocellular carcinoma by restoring p53 signaling activity.Cell death & disease · 2020Article
- Senescence-Associated Pro-inflammatory Cytokines and Tumor Cell Plasticity.Frontiers in molecular biosciences · 2020Review
- Cancer stem cells in esophageal squamous cell cancer.Oncology letters · 2019Review
- Radiation-Induced DNA Damage Cooperates with Heterozygosity of TP53 and PTEN to Generate High-Grade Gliomas.Cancer research · 2019Article
- Cancer stem-like cells directly participate in vasculogenic mimicry channels in triple-negative breast cancer.Cancer biology & medicine · 2019Article
- Mitotic polarization of transcription factors during asymmetric division establishes fate of forming cancer cells.Nature communications · 2018Article
- The ribosome, (slow) beating heart of cancer (stem) cell.Oncogenesis · 2018Review
- p53 and Cell Fate: Sensitizing Head and Neck Cancer Stem Cells to Chemotherapy.Critical reviews in oncogenesis · 2018Review
- Epigenetically distinct sister chromatids and asymmetric generation of tumor initiating cells.Cell cycle (Georgetown, Tex.) · 2018Review
- Canonical and non-canonical WNT signaling in cancer stem cells and their niches: Cellular heterogeneity, omics reprogramming, targeted therapy and tumor plasticity (Review).International journal of oncology · 2017Review
- Oxidative Stress Gene Expression Profile Correlates with Cancer Patient Poor Prognosis: Identification of Crucial Pathways Might Select Novel Therapeutic Approaches.Oxidative medicine and cellular longevity · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer is a heterogeneous disease characterized by the expression of basal cell markers, no estrogen or progesterone receptor expression and a lack of HER2 overexpression. Triple-negative tumors often display activated Wnt/β-catenin signaling and most have impaired p53 function. We studied the interplay between p53 loss and Wnt/β-catenin signaling in stem cell function and tumorigenesis, by deleting p53 from the mammary epithelium of K5ΔNβcat mice displaying a constitutive activation of Wnt/β-catenin signaling in basal cells. K5ΔNβcat transgenic mice present amplification of the basal stem cell pool and develop triple-negative mammary carcinomas. The loss of p53 in K5ΔNβcat mice led to an early expansion of mammary stem/progenitor cells and accelerated the formation of triple-negative tumors. In particular, p53-deficient tumors expressed high levels of integrins and extracellular matrix components and were enriched in cancer stem cells. They also overexpressed the tyrosine kinase receptor Met, a feature characteristic of human triple-negative breast tumors. The inhibition of Met kinase activity impaired tumorsphere formation, demonstrating the requirement of Met signaling for cancer stem cell growth in this model. Human basal-like breast cancers with predicted mutated p53 status had higher levels of MET expression than tumors with wild-type p53. These results connect p53 loss and β-catenin activation to stem cell regulation and tumorigenesis in triple-negative cancer and highlight the role of Met signaling in maintaining cancer stem cell properties, revealing new cues for targeted therapies.
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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.