ArticleBreast cancer research : BCR2014
Significance of glioma-associated oncogene homolog 1 (GLI1) expression in claudin-low breast cancer and crosstalk with the nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) pathway.
Article in Breast cancer research : BCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Signaling Pathways and Natural Compounds in Triple-Negative Breast Cancer Cell Line.Molecules (Basel, Switzerland) · 2022Pooled it
- Translational drugs targeting cancer stem cells in triple-negative breast cancer.Molecular therapy. Oncology · 2025Review
- Analyzing Hedgehog pathway-related genes: insights into breast cancer tumor microenvironment and prognostic implications.Frontiers in immunology · 2025Article
- Role of EMT in drug resistance of breast cancer: molecular mechanisms and therapeutic strategies.Frontiers in oncology · 2025Review
- Advances in the Understanding of the Pathogenesis of Triple-Negative Breast Cancer.Cancer medicine · 2024Review
- Interactions between hedgehog signaling pathway and the complex tumor microenvironment in breast cancer: current knowledge and therapeutic promises.Cell communication and signaling : CCS · 2024Review
- Review
- Targeted therapy approaches for epithelial-mesenchymal transition in triple negative breast cancer.Frontiers in oncology · 2024Review
- MyD88 signaling pathways: role in breast cancer.Frontiers in oncology · 2024Review
- Hedgehog-GLI mediated control of renal formation and malformation.Frontiers in nephrology · 2023Review
- Hedgehog Pathway Inhibitors as Targeted Cancer Therapy and Strategies to Overcome Drug Resistance.International journal of molecular sciences · 2022Review
- Epithelial-to-Mesenchymal Transition Signaling Pathways Responsible for Breast Cancer Metastasis.Cellular and molecular bioengineering · 2022Review
- The PROTAC selectively degrading Bcl-xTheranostics · 2022Article
- Embryonic Programs in Cancer and Metastasis-Insights From the Mammary Gland.Frontiers in cell and developmental biology · 2022Review
- Article
- Review
- The Role of Smoothened-Dependent and -Independent Hedgehog Signaling Pathway in Tumorigenesis.Biomedicines · 2021Review
- Hedgehog Signaling: Implications in Cancers and Viral Infections.International journal of molecular sciences · 2021Review
- Basal Cell Carcinoma: From Pathophysiology to Novel Therapeutic Approaches.Biomedicines · 2020Review
- Lineage-specific roles of hedgehog-GLI signaling during mammalian kidney development.Pediatric nephrology (Berlin, Germany) · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
introductionThe recently identified claudin-low subtype of breast cancer is enriched for cells with stem-like and mesenchymal-like characteristics. This subtype is most often triple-negative (lacking the estrogen and progesterone receptors (ER, PR) as well as lacking epidermal growth factor 2 (HER2) amplification) and has a poor prognosis. There are few targeted treatment options available for patients with this highly aggressive type of cancer.
methodsUsing a high throughput inhibitor screen, we identified high expression of glioma-associated oncogene homolog 1 (GLI1), the effector molecule of the hedgehog (Hh) pathway, as a critical determinant of cell lines that have undergone an epithelial to mesenchymal transition (EMT).
resultsHigh GLI1 expression is a property of claudin-low cells and tumors and correlates with markers of EMT and breast cancer stem cells. Knockdown of GLI1 expression in claudin-low cell lines resulted in reduced cell viability, motility, clonogenicity, self-renewal, and reduced tumor growth of orthotopic xenografts. We observed non-canonical activation of GLI1 in claudin-low and EMT cell lines, and identified crosstalk with the NFκB pathway.
conclusionsThis work highlights the importance of GLI1 in the maintenance of characteristics of metastatic breast cancer stem cells. Remarkably, treatment with an inhibitor of the NFκB pathway reproducibly reduces GLI1 expression and protein levels. We further provide direct evidence for the binding of the NFκB subunit p65 to the GLI1 promoter in both EMT and claudin-low cell lines. Our results uncover crosstalk between NFκB and GLI1 signals and suggest that targeting these pathways may be effective against the claudin-low breast cancer subtype.
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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.