ArticleCancer research2011
Endoglin regulates cancer-stromal cell interactions in prostate tumors.
Article in Cancer research, 2011. 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 35 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Endoglin/CD105-Based Imaging of Cancer and Cardiovascular Diseases: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Endoglin mediates the tumor- and metastasis-promoting traits of stromal myofibroblasts in human breast carcinomas.Molecular oncology · 2025Article
- Tumoral CD105 promotes immunosuppression, metastasis, and angiogenesis in renal cell carcinoma.Cancer immunology, immunotherapy : CII · 2023Article
- Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles.Advances in experimental medicine and biology · 2023Article
- Endoglin and squamous cell carcinomas.Frontiers in medicine · 2023Article
- Can serum endoglin be used to improve the diagnostic performance in prostate cancer?World journal of urology · 2021Article
- Review
- Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021Review
- Targeting Endoglin Expressing Cells in the Tumor Microenvironment Does Not Inhibit Tumor Growth in a Pancreatic Cancer Mouse Model.OncoTargets and therapy · 2021Article
- PHOSPHO1 is a skeletal regulator of insulin resistance and obesity.BMC biology · 2020Article
- Endoglin: Beyond the Endothelium.Biomolecules · 2020Review
- Cancer-associated fibroblast regulation of tumor neo-angiogenesis as a therapeutic target in cancer.Oncology letters · 2019Review
- Comprehensive Analysis of Copy Number Variations in Kidney Cancer by Single-Cell Exome Sequencing.Frontiers in genetics · 2019Article
- Article
- Hepatocellular Carcinoma in a Patient with Hereditary Hemorrhagic Telangiectasia.Internal medicine (Tokyo, Japan) · 2018Article
- Cancer incidence in patients with hereditary hemorrhagic telangiectasia.Journal of cancer research and clinical oncology · 2017Article
- Endoglin targeting inhibits tumor angiogenesis and metastatic spread in breast cancer.Oncogene · 2016Article
- Small bowel adenocarcinoma arising in a patient with hereditary hemorrhagic telangiectasia: A case report.Oncology letters · 2016Article
- Microvascular density and immunohistochemical expression of VEGF, VEGFR-1 and VEGFR-2 in benign prostatic hyperplasia, high-grade prostate intraepithelial neoplasia and prostate cancer.Central European journal of urology · 2016Article
- Endoglin is required in Pax3-derived cells for embryonic blood vessel formation.Developmental biology · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Endoglin is an accessory receptor for TGF-β that has been implicated in prostate cancer cell detachment, migration, and invasiveness. However, the pathophysiologic significance of endoglin with respect to prostate tumorigenesis has yet to be fully established. In this study, we addressed this question by investigation of endoglin-dependent prostate cancer progression in a TRAMP (transgenic adenocarcinoma mouse prostate) mouse model where endoglin was genetically deleted. In this model, endoglin was haploinsufficient such that its allelic deletion slightly increased the frequency of tumorigenesis, yet produced smaller, less vascularized, and less metastatic tumors than TRAMP control tumors. Most strikingly, TRAMP:eng(+/-)-derived tumors lacked the pronounced infiltration of carcinoma-associated fibroblasts (CAF) that characterize TRAMP prostate tumors. Studies in human primary prostate-derived stromal cells (PrSC) confirmed that suppressing endoglin expression decreased cell proliferation, the ability to recruit endothelial cells, and the ability to migrate in response to tumor cell-conditioned medium. We found increased levels of secreted insulin-like growth factor-binding proteins (IGFBP) in the conditioned medium from endoglin-deficient PrSCs and that endoglin-dependent regulation of IGFBP-4 secretion was crucial for stromal cell-conditioned media to stimulate prostate tumor cell growth. Together, our results firmly establish the pathophysiologic involvement of endoglin in prostate cancer progression; furthermore, they show how endoglin acts to support the viability of tumor-infiltrating CAFs in the tumor microenvironment to promote neovascularization and growth.
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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.