ArticleCancer research2013
Definition of molecular determinants of prostate cancer cell bone extravasation.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 75 citations in OpenAlex.
- Circulating tumor cells from prostate cancer patients interact with E-selectin under physiologic blood flow.PloS one · 2013Trial
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- Realizing the promise of 'La Dolce Vita' via chemical biology: glycan-motif editing of sLeThe FEBS journal · 2025Review
- Circulating Tumor Microenvironment in Metastasis.Cancer research · 2025Review
- Mechanical Loading of Osteocytes via Oscillatory Fluid Flow Regulates Early-Stage PC-3 Prostate Cancer Metastasis to Bone.Advanced biology · 2025Article
- Invasion and metastasis in cancer: molecular insights and therapeutic targets.Signal transduction and targeted therapy · 2025Review
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- The role of galectins in mediating the adhesion of circulating cells to vascular endothelium.Frontiers in immunology · 2024Review
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- Mechanobiology and survival strategies of circulating tumor cells: a process towards the invasive and metastatic phenotype.Frontiers in cell and developmental biology · 2023Review
- Cancer metastasis chemoprevention prevents circulating tumour cells from germination.Signal transduction and targeted therapy · 2022Review
- Targeting HECTD3-IKKα axis inhibits inflammation-related metastasis.Signal transduction and targeted therapy · 2022Article
- Fucosylation in Urological Cancers.International journal of molecular sciences · 2021Review
- Review
- Probing Intravascular Adhesion and Extravasation of Tumor Cells with Microfluidics.Methods in molecular biology (Clifton, N.J.) · 2021Article
- The Heterogeneity of Neutrophil Recruitment in the Tumor Microenvironment and the Formation of Premetastatic Niches.Journal of immunology research · 2021Review
- MicroRNA-92a Targets SERTAD3 and Regulates the Growth, Invasion, and Migration of Prostate Cancer Cells via the P53 Pathway.OncoTargets and therapy · 2020Article
- Cancer immunotherapy needs to learn how to stick to its guns.The Journal of clinical investigation · 2019Article
- I-branched carbohydrates as emerging effectors of malignant progression.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Glycosylation in the Tumor Microenvironment: Implications for Tumor Angiogenesis and Metastasis.Cells · 2019Review
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
Abstract
Advanced prostate cancer commonly metastasizes to bone, but transit of malignant cells across the bone marrow endothelium (BMEC) remains a poorly understood step in metastasis. Prostate cancer cells roll on E-selectin(+) BMEC through E-selectin ligand-binding interactions under shear flow, and prostate cancer cells exhibit firm adhesion to BMEC via β1, β4, and αVβ3 integrins in static assays. However, whether these discrete prostate cancer cell-BMEC adhesive contacts culminate in cooperative, step-wise transendothelial migration into bone is not known. Here, we describe how metastatic prostate cancer cells breach BMEC monolayers in a step-wise fashion under physiologic hemodynamic flow. Prostate cancer cells tethered and rolled on BMEC and then firmly adhered to and traversed BMEC via sequential dependence on E-selectin ligands and β1 and αVβ3 integrins. Expression analysis in human metastatic prostate cancer tissue revealed that β1 was markedly upregulated compared with expression of other β subunits. Prostate cancer cell breaching was regulated by Rac1 and Rap1 GTPases and, notably, did not require exogenous chemokines as β1, αVβ3, Rac1, and Rap1 were constitutively active. In homing studies, prostate cancer cell trafficking to murine femurs was dependent on E-selectin ligand, β1 integrin, and Rac1. Moreover, eliminating E-selectin ligand-synthesizing α1,3 fucosyltransferases in transgenic adenoma of mouse prostate mice dramatically reduced prostate cancer incidence. These results unify the requirement for E-selectin ligands, α1,3 fucosyltransferases, β1 and αVβ3 integrins, and Rac/Rap1 GTPases in mediating prostate cancer cell homing and entry into bone and offer new insight into the role of α1,3 fucosylation in prostate cancer development.
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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.