ArticleMolecular cancer research : MCR2011
Macrophage-dependent cleavage of the laminin receptor α6β1 in prostate cancer.
Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Macrophages and Urokinase Plasminogen Activator Receptor System in Multiple Myeloma: Case Series and Literature Review.International journal of molecular sciences · 2023Review
- The Roles of Tumor-Associated Macrophages in Prostate Cancer.Journal of oncology · 2022Review
- Role of secreted extracellular nicotinamide phosphoribosyltransferase (eNAMPT) in prostate cancer progression: Novel biomarker and therapeutic target.EBioMedicine · 2020Article
- Non-genomic Actions of Thyroid Hormones Regulate the Growth and Angiogenesis of T Cell Lymphomas.Frontiers in endocrinology · 2019Review
- The Identification of Macrophage-enriched Glycoproteins Using Glycoproteomics.Molecular & cellular proteomics : MCP · 2017Article
- Translational Significance for Tumor Metastasis of Tumor-Associated Macrophages and Epithelial-Mesenchymal Transition.Frontiers in immunology · 2017Review
- The Cohesive Metastasis Phenotype in Human Prostate Cancer.Biochimica et biophysica acta · 2016Review
- Synergistic immunologic targets for the treatment of prostate cancer.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- Schwann Cells Increase Prostate and Pancreatic Tumor Cell Invasion Using Laminin Binding A6 Integrin.Journal of cellular biochemistry · 2016Article
- Hypoxia-inducible factor-1α and Wnt/β-catenin signaling pathways promote the invasion of hypoxic gastric cancer cells.Molecular medicine reports · 2015Article
- Immunostimulatory early phenotype of tumor-associated macrophages does not predict tumor growth outcome in an HLA-DR mouse model of prostate cancer.Cancer immunology, immunotherapy : CII · 2015Article
- Intracellular modifiers of integrin alpha 6p production in aggressive prostate and breast cancer cell lines.Biochemical and biophysical research communications · 2014Article
- Senescent remodeling of the innate and adaptive immune system in the elderly men with prostate cancer.Current gerontology and geriatrics research · 2014Review
- Article
- Integrin α3β1 regulates tumor cell responses to stromal cells and can function to suppress prostate cancer metastatic colonization.Clinical & experimental metastasis · 2013Article
- RGD-Binding Integrins in Prostate Cancer: Expression Patterns and Therapeutic Prospects against Bone Metastasis.Cancers · 2012Article
- Akt1 mediates prostate cancer cell microinvasion and chemotaxis to metastatic stimuli via integrin β₃ affinity modulation.British journal of cancer · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The laminin-binding integrin α6β1 plays a major role in determining the aggressive phenotype of tumor cells during metastasis. Our previous work has shown that cleavage of the α6β1 integrin to produce the structural variant α6pβ1 on tumor cell surfaces is mediated by the serine protease urokinase plasminogen activator (uPA). Cleavage of α6β1 increases tumor cell motility, invasion, and prostate cancer metastasis, and blockage of uPA inhibits α6pβ1 production. In human tumors, uPA and uPAR are expressed in tumor cells and tumor-associated macrophages (TAM). TAMs localize to solid tumors and contribute to increased tumor growth and the metastatic phenotype. In this study, we utilized a coculture system of PC-3 prostate tumor cells and macrophages [12-O-tetradecanoylphorbol-13-acetate (TPA)-differentiated human leukemia HL-60 cells] to investigate the hypothesis that macrophages stimulate the production of the prometastatic variant α6pβ1 on human prostate cancer cells via the uPA/uPAR axis. Our results indicate that adherent macrophages cocultured with PC-3 cells increased PC-3 uPAR mRNA, uPAR cell surface protein expression and α6 integrin cleavage. The stimulation does not require macrophage/tumor cell contact because macrophage conditioned medium is sufficient for increased uPAR transcription and α6 cleavage-dependent PC-3 cell invasion. The increased cleavage was dependent on uPAR because production was blocked by silencing RNA-targeting uPAR. These results indicate that macrophages can stimulate uPA/uPAR production in tumor cells which results in α6 integrin cleavage. These data suggest that TAMs promote prometastatic integrin-dependent pericellular proteolysis.
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Registered trials
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