ArticleCancer research2011
Angiocrine factors modulate tumor proliferation and motility through EphA2 repression of Slit2 tumor suppressor function in endothelium.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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, 58 citations in OpenAlex.
- Article
- Targeting the tumour vasculature: from vessel destruction to promotion.Nature reviews. Cancer · 2024Review
- The crossroad between tumor and endothelial cells.Clinical and experimental medicine · 2024Review
- Regulation of fatty acid delivery to metastases by tumor endothelium.bioRxiv : the preprint server for biology · 2024Article
- Endothelial cells in tumor microenvironment: insights and perspectives.Frontiers in immunology · 2024Review
- Exploring the crosstalk between endothelial cells, immune cells, and immune checkpoints in the tumor microenvironment: new insights and therapeutic implications.Cell death & disease · 2023Review
- Article
- Suprabasin: Role in human cancers and other diseases.Molecular biology reports · 2022Review
- Control of Tumor Progression by Angiocrine Factors.Cancers · 2021Review
- Article
- Angiocrine Regulation of Epithelial Barrier Integrity in Inflammatory Bowel Disease.Frontiers in medicine · 2021Review
- Structural insights and evaluation of the potential impact of missense variants on the interactions of SLIT2 with ROBO1/4 in cancer progression.Scientific reports · 2020Article
- The Epigenetic Profile of Tumor Endothelial Cells. Effects of Combined Therapy with Antiangiogenic and Epigenetic Drugs on Cancer Progression.International journal of molecular sciences · 2020Review
- Article
- Tumor Endothelial Cells (TECs) as Potential Immune Directors of the Tumor Microenvironment - New Findings and Future Perspectives.Frontiers in cell and developmental biology · 2020Review
- Tumor Endothelial Heterogeneity in Cancer Progression.Cancers · 2019Review
- Vascular beds maintain pancreatic tumour explants for ex vivo drug screening.Journal of tissue engineering and regenerative medicine · 2018Article
- Targeting EphA2 impairs cell cycle progression and growth of basal-like/triple-negative breast cancers.Oncogene · 2017Article
- Tumor endothelial cells accelerate tumor metastasis.Cancer science · 2017Review
- Lipophilic siRNA targets albumin in situ and promotes bioavailability, tumor penetration, and carrier-free gene silencing.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
It is well known that tumor-derived proangiogenic factors induce neovascularization to facilitate tumor growth and malignant progression. However, the concept of "angiocrine" signaling, in which signals produced by endothelial cells elicit tumor cell responses distinct from vessel function, has been proposed, yet remains underinvestigated. Here, we report that angiocrine factors secreted from endothelium regulate tumor growth and motility. We found that Slit2, which is negatively regulated by endothelial EphA2 receptor, is one such tumor suppressive angiocrine factor. Slit2 activity is elevated in EphA2-deficient endothelium. Blocking Slit activity restored angiocrine-induced tumor growth/motility, whereas elevated Slit2 impaired growth/motility. To translate our findings to human cancer, we analyzed EphA2 and Slit2 expression in human cancer. EphA2 expression inversely correlated with Slit2 in the vasculature of invasive human ductal carcinoma samples. Moreover, analysis of large breast tumor data sets revealed that Slit2 correlated positively with overall and recurrence-free survival, providing clinical validation for the tumor suppressor function for Slit2 in human breast cancer. Together, these data support a novel, clinically relevant mechanism through which EphA2 represses Slit2 expression in endothelium to facilitate angiocrine-mediated tumor growth and motility by blocking a tumor suppressive signal.
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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.