ArticleStem cells (Dayton, Ohio)2015
Development of a Fluorescent Reporter System to Delineate Cancer Stem Cells in Triple-Negative Breast Cancer.
Article in Stem cells (Dayton, Ohio), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 80 citations in OpenAlex.
- Glycolytic enolase 1-induced H4K12 lactylation activates quiescent breast cancer stem-like cells in triple-negative breast cancer.Signal transduction and targeted therapy · 2026Article
- Establishing the first Afro-Caribbean breast cancer cell lines reveals ECM pathway enrichment and distinctive drug sensitivities.Scientific reports · 2026Article
- The role of Junctional Adhesion Molecule-A (JAM-A) in breast cancer metastasis.Molecular biology reports · 2026Review
- The role of pluripotency regulators in triple-negative breast cancer immune response.Frontiers in genetics · 2026Review
- Spatial self-organization of cancer stem cell niches revealed by live single-cell imaging.Stem cell research & therapy · 2025Article
- Phosphoproteomic Changes Induced by Cell-Derived Matrix and Their Effect on Tumor Cell Migration and Cytoskeleton Remodeling.ACS biomaterials science & engineering · 2023Article
- Endothelial cells metabolically regulate breast cancer invasion toward a microvessel.APL bioengineering · 2023Article
- Targeting ABCA12-controlled ceramide homeostasis inhibits breast cancer stem cell function and chemoresistance.Science advances · 2023Article
- MUC1-C integrates aerobic glycolysis with suppression of oxidative phosphorylation in triple-negative breast cancer stem cells.iScience · 2023Article
- Bone-matrix mineralization dampens integrin-mediated mechanosignalling and metastatic progression in breast cancer.Nature biomedical engineering · 2023Article
- Triple negative breast cancer metastasis is hindered by a peptide antagonist of F11R/JAM‑A protein.Cancer cell international · 2023Article
- Therapeutic implications of cancer stem cells in prostate cancer.Cancer biology & medicine · 2023Review
- Convergent Approaches to Delineate the Metabolic Regulation of Tumor Invasion by Hyaluronic Acid Biosynthesis.Advanced healthcare materials · 2023Article
- Silencing Notch4 promotes tumorigenesis and inhibits metastasis of triple-negative breast cancer via Nanog and Cdc42.Cell death discovery · 2023Article
- Differential contractility regulates cancer stem cell migration.Biophysical journal · 2023Article
- Spatiotemporal dissection of tumor microenvironment via in situ sensing and monitoring in tumor-on-a-chip.Biosensors & bioelectronics · 2023Article
- Kruppel-like factor 8 regulates triple negative breast cancer stem cell-like activity.Frontiers in oncology · 2023Article
- The F11 Receptor (F11R)/Junctional Adhesion Molecule-A (JAM-A) (F11R/JAM-A) in cancer progression.Molecular and cellular biochemistry · 2022Review
- Reporter gene systems for the identification and characterization of cancer stem cells.World journal of stem cells · 2021Review
- Markers and Reporters to Reveal the Hierarchy in Heterogeneous Cancer Stem Cells.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Advanced cancers display cellular heterogeneity driven by self-renewing, tumorigenic cancer stem cells (CSCs). The use of cell lines to model CSCs is challenging due to the difficulty of identifying and isolating cell populations that possess differences in self-renewal and tumor initiation. To overcome these barriers in triple-negative breast cancer (TNBC), we developed a CSC system using a green fluorescent protein (GFP) reporter for the promoter of the well-established pluripotency gene NANOG. NANOG-GFP+ cells gave rise to both GFP+ and GFP(-) cells, and GFP+ cells possessed increased levels of the embryonic stem cell transcription factors NANOG, SOX2, and OCT4 and elevated self-renewal and tumor initiation capacities. GFP+ cells also expressed mesenchymal markers and demonstrated increased invasion. Compared with the well-established CSC markers CD24(-) /CD44(+) , CD49f, and aldehyde dehydrogenase (ALDH) activity, our NANOG-GFP reporter system demonstrated increased enrichment for CSCs. To explore the utility of this system as a screening platform, we performed a flow cytometry screen that confirmed increased CSC marker expression in the GFP+ population and identified new cell surface markers elevated in TNBC CSCs, including junctional adhesion molecule-A (JAM-A). JAM-A was highly expressed in GFP+ cells and patient-derived xenograft ALDH+ CSCs compared with the GFP(-) and ALDH(-) cells, respectively. Depletion of JAM-A compromised self-renewal, whereas JAM-A overexpression induced self-renewal in GFP(-) cells. Our data indicate that we have defined and developed a robust system to monitor differences between CSCs and non-CSCs in TNBC that can be used to identify CSC-specific targets for the development of future therapeutic strategies.
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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.