ArticleCancer research2010
Shedding of RANKL by tumor-associated MT1-MMP activates Src-dependent prostate cancer cell migration.
Article in Cancer research, 2010. 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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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
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- The Role of the Metzincin Superfamily in Prostate Cancer Progression: A Systematic-Like Review.International journal of molecular sciences · 2021Pooled it
- The interrelationship between prostate cancer and osteoporosis: new perspectives on shared molecular pathways and treatment strategies.International journal of surgery (London, England) · 2026Article
- Cancer-Associated Fibroblasts in Prostate Cancer: Unraveling Mechanisms and Therapeutic Implications.Oncology research · 2026Review
- The Role of Membrane-Type 1 Matrix Metalloproteinase-Substrate Interactions in Pathogenesis.International journal of molecular sciences · 2023Review
- The RANK/RANKL/OPG system and tumor bone metastasis: Potential mechanisms and therapeutic strategies.Frontiers in endocrinology · 2022Review
- Genetic association of MMP14 promoter variants and their functional significance in gallbladder cancer pathogenesis.Journal of human genetics · 2021Article
- Targeting Extracellular Matrix Remodeling Restores BRAF Inhibitor Sensitivity in BRAFi-resistant Melanoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Effects of the Bone/Bone Marrow Microenvironments on Prostate Cancer Cells and CD59 Expression.BioMed research international · 2020Article
- Destroy to Rebuild: The Connection Between Bone Tissue Remodeling and Matrix Metalloproteinases.Frontiers in physiology · 2020Review
- Primary prostate cancer educates bone stroma through exosomal pyruvate kinase M2 to promote bone metastasis.The Journal of experimental medicine · 2019Article
- Translocating a High-Affinity Designer TIMP-1 to the Cell Membrane for Total Renal Carcinoma Inhibition: Putting the Prion Protein to Good Use.Molecular and cellular biology · 2019Article
- Contribution of the plasma and lymph Degradome and Peptidome to the MHC Ligandome.Immunogenetics · 2019Review
- The membrane tethered matrix metalloproteinase MT1-MMP triggers an outside-in DNA damage response that impacts chemo- and radiotherapy responses of breast cancer.Cancer letters · 2019Article
- Targeting a Designer TIMP-1 to the Cell Surface for Effective MT1-MMP Inhibition: A Potential Role for the Prion Protein in Renal Carcinoma Therapy.Molecules (Basel, Switzerland) · 2019Article
- Cutting to the Chase: How Matrix Metalloproteinase-2 Activity Controls Breast-Cancer-to-Bone Metastasis.Cancers · 2018Review
- MMP14 is a novel target of PTH signaling in osteocytes that controls resorption by regulating soluble RANKL production.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Dioxin Exposure in the Manufacture of Pesticide Production as a Risk Factor for Death from Prostate Cancer: A Meta-analysis.Iranian journal of public health · 2018Review
- Small leucine rich proteoglycans, a novel link to osteoclastogenesis.Scientific reports · 2017Article
- Article
- Immune mediators in the tumor microenvironment of prostate cancer.Chinese journal of cancer · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Membrane type 1 matrix metalloproteinase (MT1-MMP) plays an essential role in protease-mediated extracellular matrix (ECM) degradation, but it also functions as a sheddase releasing non-ECM substrates such as receptor activator of NF-kappaB ligand (RANKL), an osteoclastogenic factor typically confined to the surface of osteoblasts. We previously found high expression of MT1-MMP in skeletal metastasis of prostate cancer patients, in a pattern similar to RANKL expression. We also showed that overexpression of MT1-MMP in prostate cancer cells increases tumor growth and osteolysis in an intratibial mouse model of bone metastasis, and that soluble factor(s) shed by tumor-derived MT1-MMP enhance osteoclast differentiation in a RANKL-dependent manner. Recent evidence indicates that the cognate receptor for RANKL, RANK, is expressed in prostate cancer cells, suggesting the presence of an autocrine pathway. In this study, we show that MT1-MMP-expressing LNCaP prostate cancer cells display enhanced migration. Moreover, conditioned medium from LNCaP cells expressing both RANKL and MT1-MMP stimulates the migration of MT1-MMP-deficient C42b prostate cancer cells. This enhanced chemotaxis can be abrogated by osteoprotegerin (soluble decoy receptor of RANKL), MIK-G2 (a selective inhibitor for MT1-MMP), and PP2 (a Src inhibitor). These findings indicate that tumor-derived MT1-MMP enhances tumor cell migration through initiation of an autocrine loop requiring ectodomain shedding of membrane-bound RANKL in prostate cancer cells, and that Src is a key downstream mediator of RANKL-induced migration of prostate cancer cells.
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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.