ReviewInternational journal of molecular sciences2022
Addiction of Cancer Stem Cells to MUC1-C in Triple-Negative Breast Cancer Progression.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 35 citations in OpenAlex.
- Evolution ofInternational journal of molecular sciences · 2026Review
- Evolution of the MUC1 gene in eutherian mammals as an adaptation responsible for the increasing incidence of cancer in humans.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- GCNT3 and ST3GAL1 expression correlates with HER2 status and MUC1/β-catenin/Cyclin D1 axis in breast cancer.BMC cancer · 2026Article
- Targeted biologics for TNBC: Advances in nanobodies, antibodies, peptides, and aptamers.Molecular therapy. Oncology · 2026Review
- Artemis: Harnessing Knowledge Graphs for Next-Generation Drug Target Prioritization.Computational and structural biotechnology journal · 2026Article
- Knockout of Mucin 1 inhibits the proliferation, migration, and invasion of human MDA-MB-231 cells by blocking autophagy flow.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Article
- In silico design of a multi-epitope vaccine against the triple negative breast cancer.Scientific reports · 2025Article
- MUC1-C auto-regulatory complex with EBNA1 is responsible for latent Epstein-Barr virus-associated gastric cancer progression.Oncogene · 2025Article
- MUC1-C dependency in drug resistant HR+/HER2- breast cancer identifies a new target for antibody-drug conjugate treatment.NPJ breast cancer · 2025Article
- Research progress of MUC1 in genitourinary cancers.Cellular & molecular biology letters · 2024Review
- A mini-review-cancer energy reprogramming on drug resistance and immune response.Translational oncology · 2024Review
- MUC1-C regulates NEAT1 lncRNA expression and paraspeckle formation in cancer progression.Oncogene · 2024Article
- The Role of MUC1 in Renal Cell Carcinoma.Biomolecules · 2024Review
- Article
- MUC1-C is a target of salinomycin in inducing ferroptosis of cancer stem cells.Cell death discovery · 2024Article
- The molecular determinants of phenotypic plasticity in homeostasis and neoplasia.Cancer heterogeneity and plasticity · 2024Article
- The mechanism underlying metastasis in triple-negative breast cancer: focusing on the interplay between ferroptosis, epithelial-mesenchymal transition, and non-coding RNAs.Frontiers in pharmacology · 2024Review
- Patterns of immune evasion in triple-negative breast cancer and new potential therapeutic targets: a review.Frontiers in immunology · 2024Review
- MUC1-C integrates aerobic glycolysis with suppression of oxidative phosphorylation in triple-negative breast cancer stem cells.iScience · 2023Article
- MUC1-C intersects chronic inflammation with epigenetic reprogramming by regulating the set1a compass complex in cancer progression.Communications biology · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) is an aggressive malignancy with limited treatment options. TNBC progression is associated with expansion of cancer stem cells (CSCs). Few insights are available regarding druggable targets that drive the TNBC CSC state. This review summarizes the literature on TNBC CSCs and the compelling evidence that they are addicted to the MUC1-C transmembrane protein. In normal epithelia, MUC1-C is activated by loss of homeostasis and induces reversible wound-healing responses of inflammation and repair. However, in settings of chronic inflammation, MUC1-C promotes carcinogenesis. MUC1-C induces EMT, epigenetic reprogramming and chromatin remodeling in TNBC CSCs, which are dependent on MUC1-C for self-renewal and tumorigenicity. MUC1-C-induced lineage plasticity in TNBC CSCs confers DNA damage resistance and immune evasion by chronic activation of inflammatory pathways and global changes in chromatin architecture. Of therapeutic significance, an antibody generated against the MUC1-C extracellular domain has been advanced in a clinical trial of anti-MUC1-C CAR T cells and in IND-enabling studies for development as an antibody-drug conjugate (ADC). Agents targeting the MUC1-C cytoplasmic domain have also entered the clinic and are undergoing further development as candidates for advancing TNBC treatment. Eliminating TNBC CSCs will be necessary for curing this recalcitrant cancer and MUC1-C represents a promising druggable target for achieving that goal.
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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.