ArticleMolecular biology of the cell2013
Targeted inactivation of β1 integrin induces β3 integrin switching, which drives breast cancer metastasis by TGF-β.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 62 papers.
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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.
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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
62 citing papers in PubMed, 95 citations in OpenAlex.
- ITGB1 Regulates Triple-Negative Breast Cancer Development by Modulating the Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transforming growth factor-β and integrins: key players in EMT and breast cancer progression.Cancer cell international · 2026Review
- K562 Chronic Myeloid Leukemia Cells as a Dual β3-Expressing Functional Cell Line Model to Investigate the Effects of Combined αIIbβ3 and αvβ3 Antagonism.Methods and protocols · 2025Article
- Interplay of integrins and selectins in metastasis.Molecular oncology · 2025Review
- Article
- Cilengitide sensitivity is predicted by overall integrin expression in breast cancer.Breast cancer research : BCR · 2024Article
- Family-Wide Photoproximity Profiling of Integrin Protein Social Networks in Cancer.bioRxiv : the preprint server for biology · 2024Article
- TGF-β signaling: critical nexus of fibrogenesis and cancer.Journal of translational medicine · 2024Review
- Development of a Novel, Potent, and Selective Sialyltransferase Inhibitor for Suppressing Cancer Metastasis.International journal of molecular sciences · 2024Article
- Neuropilin-1 Knockout and Rescue Confirms Its Role to Promote Metastasis in MDA-MB-231 Breast Cancer Cells.International journal of molecular sciences · 2023Article
- Cell- and subcellular organelle-targeting nanoparticle-mediated breast cancer therapy.Frontiers in pharmacology · 2023Review
- Review
- MASTL is enriched in cancerous and pluripotent stem cells and influences OCT1/OCT4 levels.iScience · 2022Article
- Review
- The interactions between integrin αInternational journal of biological sciences · 2022Article
- Mechanisms of Cell Adhesion Molecules in Endocrine-Related Cancers: A Concise Outlook.Frontiers in endocrinology · 2022Review
- Biological Mechanisms and Therapeutic Opportunities in Mammographic Density and Breast Cancer Risk.Cancers · 2021Review
- Integrins as attractive targets for cancer therapeutics.Acta pharmaceutica Sinica. B · 2021Review
- Biphasic α2β1 Integrin Expression in Breast Cancer Metastasis to Bone.International journal of molecular sciences · 2021Article
- Prognostic value of the PrPOncoimmunology · 2021Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mammary tumorigenesis and epithelial-mesenchymal transition (EMT) programs cooperate in converting transforming growth factor-β (TGF-β) from a suppressor to a promoter of breast cancer metastasis. Although previous reports associated β1 and β3 integrins with TGF-β stimulation of EMT and metastasis, the functional interplay and plasticity exhibited by these adhesion molecules in shaping the oncogenic activities of TGF-β remain unknown. We demonstrate that inactivation of β1 integrin impairs TGF-β from stimulating the motility of normal and malignant mammary epithelial cells (MECs) and elicits robust compensatory expression of β3 integrin solely in malignant MECs, but not in their normal counterparts. Compensatory β3 integrin expression also 1) enhances the growth of malignant MECs in rigid and compliant three-dimensional organotypic cultures and 2) restores the induction of the EMT phenotypes by TGF-β. Of importance, compensatory expression of β3 integrin rescues the growth and pulmonary metastasis of β1 integrin-deficient 4T1 tumors in mice, a process that is prevented by genetic depletion or functional inactivation of β3 integrin. Collectively our findings demonstrate that inactivation of β1 integrin elicits metastatic progression via a β3 integrin-specific mechanism, indicating that dual β1 and β3 integrin targeting is necessary to alleviate metastatic disease in breast cancer patients.
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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.