ArticleAngiogenesis2011
Vascular endothelial growth inhibitor (VEGI; TNFSF15) inhibits bone marrow-derived endothelial progenitor cell incorporation into Lewis lung carcinoma tumors.
Article in Angiogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 38 citations in OpenAlex.
- TNFSF15 alleviates myeloid-derived suppressor cell-mediated cancer immunosuppression in mice.Acta pharmacologica Sinica · 2026Article
- The genomic landscape of the immune system in lung cancer: present insights and continuing investigations.Frontiers in genetics · 2024Review
- TNFSF15 facilitates the differentiation of CD11bCancer biology & medicine · 2023Article
- Article
- VEGI downregulation is correlated with nodal metastasis and poor prognosis in lung adenocarcinoma.Molecular and clinical oncology · 2021Article
- TNFSF15 facilitates human umbilical cord blood haematopoietic stem cell expansion by activating Notch signal pathway.Journal of cellular and molecular medicine · 2020Article
- TNFSF15 promoter polymorphisms increase the susceptibility to small cell lung cancer: a case-control study.BMC medical genetics · 2019Article
- Vascular endothelial growth factor suppresses TNFSF15 production in endothelial cells by stimulating miR-31 and miR-20a expression via activation of Akt and Erk signals.FEBS open bio · 2017Article
- A case-control study about the association between vascular endothelial growth inhibitor gene polymorphisms and breast cancer risk in female patients in Northeast China.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2016Article
- EphA1 activation promotes the homing of endothelial progenitor cells to hepatocellular carcinoma for tumor neovascularization through the SDF-1/CXCR4 signaling pathway.Journal of experimental & clinical cancer research : CR · 2016Article
- TNFSF15 inhibits vasculogenesis by regulating relative levels of membrane-bound and soluble isoforms of VEGF receptor 1.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- TNFSF15 Modulates Neovascularization and Inflammation.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2012Article
- In vitro labeling of endothelial progenitor cells isolated from peripheral blood with superparamagnetic iron oxide nanoparticles.Molecular medicine reports · 2012Article
- Advancement in the research on vascular endothelial growth inhibitor (VEGI).Targeted oncology · 2012Review
- Counterbalance: modulation of VEGF/VEGFR activities by TNFSF15.Signal transduction and targeted therapyArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Bone marrow (BM)-derived endothelial progenitor cells (EPC) have a critical role in tumor neovascularization. Vascular endothelial growth inhibitor (VEGI) is a member of the TNF superfamily (TNFSF15). We have shown that recombinant VEGI suppresses tumor angiogenesis by specifically eliminating proliferating endothelial cells (EC). We report here that treatment of tumor bearing mice with recombinant VEGI leads to a significantly decreased population of BM-derived EPC in the tumors. We transplanted whole bone marrow from green fluorescent protein (GFP) transgenic mice into C57BL/6 recipient mice, which were then inoculated with Lewis lung carcinoma (LLC) cells. Intraperitoneal injection of recombinant VEGI led to significant inhibition of tumor growth and decrease of vasculature density compared to vehicle-treated mice. Tumor implantation yielded a decrease of BM-derived EPC in the peripheral blood, while VEGI-treatment resulted in an initial delay of such decrease. Analysis of the whole bone marrow showed a decrease of Lin(-)-c-Kit(+)-Sca-1(+) hematopoietic stem cell (HSC) population in tumor bearing mice; however, VEGI-treatment caused a significant increase of this cell population. In addition, the number of BM-derived EPC in VEGI-treated tumors was notably less than that in the vehicle-treated group, and most of the apoptotic cells in the VEGI-treated tumors were of bone marrow origin. These findings indicate that VEGI inhibits BM-derived EPC mobilization and prevents their incorporation into LLC tumors by inducing apoptosis specifically of BM-derived cells, resulting in the inhibition of EPC-supported tumor vasculogenesis and tumor growth.
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