ArticlePloS one2015
β-Catenin is required for the tumorigenic behavior of triple-negative breast cancer cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 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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Who cites it
120 citing papers in PubMed, 176 citations in OpenAlex.
- THBS2: the key hub linking breast cancer stroma, immunity, and therapeutic response.Clinical & experimental metastasis · 2026Review
- DP103 as a critical modulator of Wnt signaling and cancer stemness: implications for precision treatment in triple negative breast cancer.Cell death & disease · 2026Article
- Extracellular vesicles inherit lactate from aggregated MSCs to alleviate type 1 diabetes mellitus via HJournal of nanobiotechnology · 2026Article
- KRT17 promotes triple negative breast cancer through activation of Wnt signaling and γδ T-cells recruitment.Communications biology · 2026Article
- Eugenoplatin (a phyto-chemo drug conjugate) targets cancer stem cells through inhibition of the β-catenin signaling in triple-negative breast cancer cells.Journal of translational medicine · 2026Article
- Emerging Approaches in Breast Cancer: From Molecular Mechanisms to Diagnosis and Therapeutic Strategies.Oncology research · 2026Review
- Research Progress on Signaling Pathways in Breast Cancer Bone Metastasis.Oncology research · 2026Review
- miRNA-195-5p modulates cell proliferation and stemness by targeting the Wnt signalling network in breast cancer.Non-coding RNA research · 2025Article
- IL-3/STAT5/miR-155-5p axis supports stem-related pathway reprogramming in TNBC.Breast cancer research : BCR · 2025Article
- Translational drugs targeting cancer stem cells in triple-negative breast cancer.Molecular therapy. Oncology · 2025Review
- Bufalin Suppresses Triple-Negative Breast Cancer Stem Cell Growth by Inhibiting the Wnt/β-Catenin Signaling Pathway.Journal of microbiology and biotechnology · 2025Article
- Role of the Wnt signaling pathway in the complex microenvironment of breast cancer and prospects for therapeutic potential (Review).International journal of oncology · 2025Review
- Divide and Conquer-Targeted Therapy for Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Review
- Wnt/β-catenin signalling underpins juvenile Fasciola hepatica growth and development.PLoS pathogens · 2025Article
- Triple-Negative Breast Cancer Progression and Drug Resistance in the Context of Epithelial-Mesenchymal Transition.Cancers · 2025Review
- Advances in the Understanding of the Pathogenesis of Triple-Negative Breast Cancer.Cancer medicine · 2024Review
- Beyond the Gut: The intratumoral microbiome's influence on tumorigenesis and treatment response.Cancer communications (London, England) · 2024Review
- BMP Stimulation Differentially Affects Phosphorylation and Protein Stability of β-Catenin in Breast Cancer Cell Lines.International journal of molecular sciences · 2024Article
- The regulation of microRNAs on chemoresistance in triple-negative breast cancer: a recent update.Epigenomics · 2024Review
- Gallic acid promotes ferroptosis in hepatocellular carcinoma via inactivating Wnt/β-catenin signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Our previous data illustrated that activation of the canonical Wnt signaling pathway was enriched in triple-negative breast cancer and associated with reduced overall survival in all patients. To determine whether Wnt signaling may be a promising therapeutic target for triple-negative breast cancer, we investigated whether β-catenin was necessary for tumorigenic behaviors in vivo and in vitro. β-catenin expression level was significantly reduced in two human triple-negative breast cancer cell lines, MDA-MB-231 and HCC38, using lentiviral delivery of β-catenin-specific small hairpin RNAs (shRNAs). Upon implantation of the cells in the mammary fat pad of immunocompromised mice, we found that β-catenin shRNA HCC38 cells formed markedly smaller tumors than control cells and grew much more slowly. In in vitro assays, β-catenin silencing significantly reduced the percentage of Aldefluor-positive cells, a read-out of the stem-like cell population, as well as the expression of stem cell-related target genes including Bmi-1 and c-Myc. β-catenin-knockdown cells were also significantly impaired in their ability to migrate in wound-filling assays and form anchorage-independent colonies in soft agar. β-catenin-knockdown cells were more sensitive to chemotherapeutic agents doxorubicin and cisplatin. Collectively, these data suggest that β-catenin is required for triple-negative breast cancer development by controlling numerous tumor-associated properties, such as migration, stemness, anchorage-independent growth and chemosensitivity.
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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.