Reduced vascular endothelial growth inhibitor (VEGI) expression is associated with poor prognosis in breast cancer patients

Parr, Christian; Gan, Chun H.; Watkins, Gareth; Jiang, Wen Guo

doi:10.1007/s10456-006-9033-1

Cited by 54 publications

(64 citation statements)

References 40 publications

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“…This was based on methods we previously described (14)(15)(16). Frozen sections of breast tumour and back-ground tissue were cut at a thickness of 6 μm using a cryostat (Leica).…”

Section: Real-time Quantitative Polymerase Chain Reaction (Q-pcr)mentioning

confidence: 99%

PGF isoforms, PLGF-1 and PGF-2 and the PGF receptor, neuropilin, in human breast cancer: Prognostic significance

Escudero-Esparza

Martin²,

Douglas-Jones³

et al. 2009

Oncol Rep

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“…This was based on methods we previously described (14)(15)(16). Frozen sections of breast tumour and back-ground tissue were cut at a thickness of 6 μm using a cryostat (Leica).…”

Section: Real-time Quantitative Polymerase Chain Reaction (Q-pcr)mentioning

confidence: 99%

PGF isoforms, PLGF-1 and PGF-2 and the PGF receptor, neuropilin, in human breast cancer: Prognostic significance

Escudero-Esparza

Martin²,

Douglas-Jones³

et al. 2009

Oncol Rep

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“…It is now known that only the solubilised extracellular domain of the three isoforms of VEGI is responsible for its biological activity (8,10,18,19,21). For example, full-length VEGI 174 was found to have no effect on tumour growth when over-expressed in cancer cells, whereas a secretable fusion protein (sVEGI) comprising a secretion signal peptide and the putative extracellular domain of VEGI 174 inhibited tumour growth when over-expressed in cancer cells (9,22,23). Table I.…”

Section: Structure Of Vegi and Vegi Isoformsmentioning

confidence: 99%

“…The process of angiogenesis involves cell proliferation, migration, tubule formation of endothelial cells, remodelling of the extracellular matrix, and invasion to surrounding tissue (30), and is tightly regulated by a balance of pro-and anti-angiogenic molecules (9,30). A number of endogenous angiogenesis inhibitors, such as angiostatin, endostatin, restin, canstatin, and tumstatin were reported and have been shown to suppress the growth of primary and metastatic tumours without affecting the normal vasculature (31).…”

Section: Vegi and Angiogenesismentioning

confidence: 99%

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Vascular endothelial growth inhibitor in human cancer (Review)

Zhang

Sanders²,

Ye³

et al. 2009

Int J Mol Med

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Abstract. Vascular endothelial growth inhibitor (VEGI), also known as tumour necrosis factor superfamily member 15 (TNFSF15) and TNF ligand related molecule 1 (TL1), is a recently identified anti-angiogenic cytokine that belongs to the TNF superfamily. Three isoforms of VEGI, VEGI 174, 192, and 251 have been documented, all sharing 151 common C-terminal amino acids but differing in their N-terminal regions. The investigations into the biological functions of VEGI have pointed to a potential cancer inhibitory role for the cytokine. The inhibitory effects of VEGI on cancer are manifested in three main areas, the direct effect on cancer cells, the anti-angiogenic effects on endothelial cells, and stimulation of maturation of dendric cells. The clinical aspect of VEGI in cancer is also being explored in recent years. The present article overviews the recent progress on this molecule and discusses the value of VEGI as a potential therapeutic target in cancer therapy. Contents1. Introduction 2. VEGI and TNF superfamily 3. Structure of VEGI and VEGI isoforms 4. Expression and cell/tissue distribution of VEGI 5. Regulation of VEGI expression 6. VEGI and angiogenesis 7. Implication of VEGI in solid tumours 8. Other functions of VEGI involved in carcinoma 9. Perspective IntroductionVascular endothelial growth inhibitor (VEGI) was first reported in 1999 from human umbilical vein endothelial cells (1,2) and was found to be identical to another gene known as tumour necrosis factor superfamily member 15 (TNFSF15) and TNF ligand related molecule 1 (TL1). The prime function of VEGI was thought to be anti-angiogenic (1,2). Originally, it was reported to be expressed exclusively in endothelial cells, but more recently VEGI 251 was found to be highly expressed in dendritic cells (DCs) after in vitro activation and in inflammatory bowel disease (IBD), particularly Crohn's disease (CD), rheumatoid arthritis, as well as renal inflammation (3-6). It was believed to be one of the evolutionarily earliest members of the TNF superfamily (7). There is evidence showing that VEGI is involved in atherogenesis. Thus, VEGI is a multipotential cytokine and plays a role in inflammation, septic shock, fever, and growth modulation through the functions of inducing apoptosis, regulating immunity, and anti-angiogenesis.Moreover, other studies demonstrated an intricate relationship between VEGI and carcinoma in vitro and in vivo (8-11). It is a potent inhibitor of endothelial cell proliferation, angiogenesis, and tumour growth (12). The present review will briefly discuss the VEGI family and focus on the impact of VEGI in cancer. VEGI and the TNF superfamilyThree decades ago, lymphotoxin (LT) and tumour necrosis factor-· (TNF) were identified as products of lymphocytes and macrophages that cause lysis of certain types of cells, especially tumour cells (13,14). The two molecules are members of a gene superfamily (15,16). There are at least 19 members so far identified within this family (Table I), which is generally referred to as tumour necrosis fact...

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“…Overexpression of VEGI-251 results in potent inhibition of endothelial cell proliferation, angiogenesis and tumor growth [10]. Reduced VEGI expression is reported to be associated with poor prognosis in breast cancer patients [11]. Other npg activities of VEGI also have been reported, including the stimulation of T-cell activation [12] and dendritic cell maturation [13].…”

Section: Introductionmentioning

confidence: 99%

VEGI-armed oncolytic adenovirus inhibits tumor neovascularization and directly induces mitochondria-mediated cancer cell apoptosis

et al. 2009

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Vascular endothelial cell growth inhibitor (VEGI) is a member of the tumor necrosis factor superfamily and plays an important role in vascular homeostasis. In this study, to investigate the anticancer therapeutic potential of this gene, a secreted isoform of VEGI (VEGI-251) was inserted into a selectively replicating adenovirus with E1B 55 kDa gene deletion (ZD55) to construct ZD55-VEGI-251. We report here that secreted VEGI-251 produced from ZD55-VEGI-251-infected cancer cells potently inhibits endothelial cell proliferation, tube formation in vitro and angiogenesis of chick chorioallantoic membrane in vivo. Additionally, ZD55-VEGI-251 infection leads to a much more severe cytopathic effect than control viruses on several human cancer cell lines, including cervical cancer cell line HeLa, hepatoma cell line SMMC-7721 and colorectal cancer cell line SW620. Further study reveals that the increased cytotoxicity is a result of VEGI-251 autocrine-dependent, mitochondria-mediated apoptosis accompanied by caspase-9 activation, enhanced caspase-3 activation and PARP cleavage. Moreover, ZD55-VEGI-251-treatment of athymic nude mice bearing human cervical and colorectal tumor xenografts markedly suppressed tumor growth. Our findings indicate that the combined effect of antiangiogenesis and apoptosis-induction activity makes the VEGI-251-armed oncolytic adenovirus a promising therapeutic agent for cancer.

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Reduced vascular endothelial growth inhibitor (VEGI) expression is associated with poor prognosis in breast cancer patients

Cited by 54 publications

References 40 publications

PGF isoforms, PLGF-1 and PGF-2 and the PGF receptor, neuropilin, in human breast cancer: Prognostic significance

PGF isoforms, PLGF-1 and PGF-2 and the PGF receptor, neuropilin, in human breast cancer: Prognostic significance

Vascular endothelial growth inhibitor in human cancer (Review)

VEGI-armed oncolytic adenovirus inhibits tumor neovascularization and directly induces mitochondria-mediated cancer cell apoptosis

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