ArticleCancer research2017
MYC Inhibition Depletes Cancer Stem-like Cells in Triple-Negative Breast Cancer.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
75 citing papers in PubMed, 134 citations in OpenAlex.
- Oncogene c‑Myc: From molecular mechanism to targeted therapy (Review).Molecular medicine reports · 2026Review
- Decoding drug-responsive cell subpopulations in triple-negative breast cancer using single-cell multiomics.iScience · 2026Article
- AnnQ: reference-based quantification of cellular abnormality at single-cell resolution.Briefings in bioinformatics · 2026Article
- Anthocyanin Derived NIR Fluorogenic Probe for Direct Visualization and Monitoring of DNA G‑Quadruplex in Breast Cancer Tumor Models.Chemical & biomedical imaging · 2026Article
- Ribosome biogenesis bottlenecks reveal vulnerabilities in cancer.bioRxiv : the preprint server for biology · 2026Article
- Obesity- and tumor-derived signals drive cancer-associated state transitions in breast mesenchymal stromal/stem cells reprogrammed by IL1RA or JAK inhibition.Experimental hematology & oncology · 2026Article
- The role of pluripotency regulators in triple-negative breast cancer immune response.Frontiers in genetics · 2026Review
- Meflin is a druggable target using antibody-drug conjugates in progressive osteosarcoma.Oncogene · 2025Article
- IL-3/STAT5/miR-155-5p axis supports stem-related pathway reprogramming in TNBC.Breast cancer research : BCR · 2025Article
- MYC/TET3-Regulated TMEM65 Activates OXPHOS-SERPINB3 Pathway to Promote Progression and Cisplatin Resistance in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A novel peptide 66CTG stabilizes Myc proto-oncogene protein to promote triple-negative breast cancer growth.Signal transduction and targeted therapy · 2025Article
- Article
- Triptolide induces apoptosis of glioma cells by inhibiting NF-κB activation during oxidative stress.Scientific reports · 2024Article
- Dual activity of Minnelide chemosensitize basal/triple negative breast cancer stem cells and reprograms immunosuppressive tumor microenvironment.Scientific reports · 2024Article
- A novel antitumor mechanism of triptonide in colorectal cancer: inducing ferroptosis via the SLC7A11/GPX4 axis.Functional & integrative genomics · 2024Article
- Triptolide and its prodrug Minnelide target high-risk MYC-amplified medulloblastoma in preclinical models.The Journal of clinical investigation · 2024Article
- C-terminally phosphorylated p27 activates self-renewal driver genes to program cancer stem cell expansion, mammary hyperplasia and cancer.Nature communications · 2024Article
- AI identifies potent inducers of breast cancer stem cell differentiation based on adversarial learning from gene expression data.Briefings in bioinformatics · 2024Article
- Nuclear localization of heparanase 2 (Hpa2) attenuates breast carcinoma growth and metastasis.Cell death & disease · 2024Article
- Article
15 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
6 authors at 1 institution in 1 country.
Funding
Abstract
There is mounting evidence that cancer stem-like cells (CSC) are selectively enriched in residual tumors after anticancer therapies, which may account for tumor recurrence and metastasis by regenerating new tumors. Thus, there is a critical need to develop new therapeutic agents that can effectively eliminate drug-resistant CSCs and improve the efficacy of cancer therapy. Here, we report that Triptolide (C1572), a small-molecule natural product, selectively depletes CSCs in a dose-dependent fashion in human triple-negative breast cancer (TNBC) cell lines. Nanomolar concentrations of C1572 markedly reduced c-MYC (MYC) protein levels via a proteasome-dependent mechanism. Silencing MYC expression phenocopied the CSC depletion effects of C1572 and induced senescence in TNBC cells. Limited dilution assays revealed that
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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.