ArticleOncotarget2014
Targeting the MUC1-C oncoprotein inhibits self-renewal capacity of breast cancer cells.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 64 citations in OpenAlex.
- The network map of mucin 1 mediated signaling in cancer progression and immune modulation.Discover oncology · 2025Article
- The Activity of Human NK Cells Towards 3D Heterotypic Cellular Tumor Model of Breast Cancer.Cells · 2025Article
- ALDH1A1 in breast cancer: A prospective target to overcome therapy resistance (Review).Oncology letters · 2025Review
- MUC1-EGFR crosstalk with IL-6 by activating NF-κB and MAPK pathways to regulate the stemness and paclitaxel-resistance of lung adenocarcinoma.Annals of medicine · 2024Article
- Multi-armored allogeneic MUC1 CAR T cells enhance efficacy and safety in triple-negative breast cancer.Science advances · 2024Article
- The multifaceted role of MUC1 in tumor therapy resistance.Clinical and experimental medicine · 2023Review
- Addiction of Cancer Stem Cells to MUC1-C in Triple-Negative Breast Cancer Progression.International journal of molecular sciences · 2022Review
- Article
- MUC1 is a potential target to overcome trastuzumab resistance in breast cancer therapy.Cancer cell international · 2022Review
- Identification of potential genes associated with ALDH1A1 overexpression and cyclophosphamide resistance in chronic myelogenous leukemia using network analysis.Medical oncology (Northwood, London, England) · 2021Article
- LncRNACancers · 2021Article
- Anti-mucin 1 chimeric antigen receptor T cells for adoptive T cell therapy of cholangiocarcinoma.Scientific reports · 2021Article
- CDYL2 Epigenetically Regulates MIR124 to Control NF-κB/STAT3-Dependent Breast Cancer Cell Plasticity.iScience · 2020Article
- Article
- ALDH1A3-regulated long non-coding RNA NRAD1 is a potential novel target for triple-negative breast tumors and cancer stem cells.Cell death and differentiation · 2020Article
- Targeting MUC1-C Inhibits TWIST1 Signaling in Triple-Negative Breast Cancer.Molecular cancer therapeutics · 2019Article
- Dual TGFβ/BMP Pathway Inhibition Enables Expansion and Characterization of Multiple Epithelial Cell Types of the Normal and Cancerous Breast.Molecular cancer research : MCR · 2019Article
- MUC1-C Integrates Chromatin Remodeling and PARP1 Activity in the DNA Damage Response of Triple-Negative Breast Cancer Cells.Cancer research · 2019Article
- STON2 negatively modulates stem-like properties in ovarian cancer cells via DNMT1/MUC1 pathway.Journal of experimental & clinical cancer research : CR · 2018Article
- Polyubiquitination inhibition of estrogen receptor alpha and its implications in breast cancer.World journal of clinical oncology · 2018Review
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 3 institutions in 2 countries.
Funding
Abstract
The capacity of breast cancer cells to form mammospheres in non-adherent serum-free culture is used as a functional characteristic of the self-renewing stem-like cell population. The present studies demonstrate that silencing expression of the MUC1-C oncoprotein inhibits growth of luminal MCF-7 and HER2-overexpressing SKBR3 breast cancer cells as mammospheres. We also show that triple-negative MDA-MB-468 breast cancer cells are dependent on MUC1-C for growth as mammospheres and tumor xenografts. Similar results were obtained when MUC1-C function was inhibited by expression of a MUC1-C(CQCAQA) mutant. Moreover, treatment with the MUC1-C inhibitor GO-203, a cell penetrating peptide that binds to the MUC1-C cytoplasmic domain and blocks MUC1-C function, confirmed the importance of this target for self-renewal. The mechanistic basis for these findings is supported by the demonstration that MUC1-C activates NF-κB, occupies the IL-8 promoter with NF-κB, and induces IL-8 transcription. MUC1-C also induces NF-κB-dependent expression of the IL-8 receptor, CXCR1. In concert with these results, targeting MUC1-C with GO-203 suppresses IL-8/CXCR1 expression and disrupts the formation of established mammospheres. Our findings indicate that MUC1-C contributes to the self-renewal of breast cancer cells by activating the NF-κBIL-8/CXCR1 pathway and that targeting MUC1-C represents a potential approach for the treatment of this population.
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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.