Vasculogenic mimicry and tumour-cell plasticity: lessons from melanoma

Hendrix, Mary J.C.; Seftor, Elisabeth A.; Hess, Angela R.; Seftor, Richard E.B.

doi:10.1038/nrc1092

Cited by 758 publications

(685 citation statements)

References 91 publications

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“…4,5 Vasculogenic mimicry is another form of vessel formation that has been reported in certain tumor types, such as aggressive human uveal melanomas, prostate and breast tumors. [6][7][8] In these cases, networks of tumor cell-lined vascular channels were identified within the tumors. Finally, vessel co-option, implemented by tumor cells as a temporary means of gaining access to a blood supply, involves the tumor cells growing around and thus co-opting existing host vessels to form an initially well-vascularized tumor.…”

mentioning

confidence: 99%

Metalloproteinases and their inhibitors in tumor angiogenesis

Handsley

Edwards

2005

Intl Journal of Cancer

263

211

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Angiogenesis is the process by which new blood vessels are formed from preexisting vasculature. It is an essential feature of the female reproductive cycle, embryonic development and wound repair. Angiogenesis has also been identified as a causal or contributing factor in several pathologies, including cancer, where it is a rate-limiting step during tumor progression. Matrix metalloproteinases (MMPs) are a family of soluble and membrane-anchored proteolytic enzymes that can degrade components of the extracellular matrix (ECM) as well as a growing number of modulators of cell function. Several of the MMPs, in particular the gelatinases and membrane-type 1 MMP (MT1-MMP), have been linked to angiogenesis. Potential roles for these proteases during the angiogenic process include degradation of the basement membrane and perivascular ECM components, unmasking of cryptic biologically relevant sites in ECM components, modulation of angiogenic factors and production of endogenous angiogenic inhibitors. This review brings together what is currently known about the functions of the MMPs and the closely related ADAM (a disintegrin and metalloproteinase domain) and ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) families in angiogenesis and considers how this information might be useful in manipulation of the angiogenic process, with a view to constraining tumor progression. ' 2005 Wiley-Liss, Inc.Key words: metalloproteinase; tumor; angiogenesis; tissue inhibitor of metalloproteinases; protease; extracellular matrix Angiogenesis is an essential feature of several physiologic processes such as the developmental growth of organs, wound healing and the female reproductive cycle. 1 It is also particularly significant in cancer progression, being a crucial step in the transition of a tumor from a hyperplastic but contained in situ state to a malignant phenotype. 2,3 To allow its growth beyond a certain critical size, a solid avascular tumor must develop its own blood supply in order to meet its growing metabolic requirements. 1 Vascularization of a tumor also provides a route for dissemination of the tumor cells to different sites around the body.Although angiogenesis appears to be the primary form of tumor vascularization, the malignant cells of a tumor can gain access to a blood supply through other means, such as via tumor-induced vasculogenesis, in which bone marrow-derived precursor endothelial cells contribute to the formation of tumor vessels. 4,5 Vasculogenic mimicry is another form of vessel formation that has been reported in certain tumor types, such as aggressive human uveal melanomas, prostate and breast tumors. [6][7][8] In these cases, networks of tumor cell-lined vascular channels were identified within the tumors. Finally, vessel co-option, implemented by tumor cells as a temporary means of gaining access to a blood supply, involves the tumor cells growing around and thus co-opting existing host vessels to form an initially well-vascularized tumor. 9 This review will highlight new insigh...

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mentioning

confidence: 99%

Metalloproteinases and their inhibitors in tumor angiogenesis

Handsley

Edwards

2005

Intl Journal of Cancer

263

211

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“…19 There have been several genes identified to be responsible for this vasculogenic phenotype including VE-cadherin, CD34, TIE2, Eph2A, LAMC2, endoglin, EDG1, ESM1 and EDF1. 20 AlphaIIb 3 transfection into v 3-expressing human melanoma cells, demonstrated here, correlated with the overexpression of certain vasculogenic genes (bFGF, CD34, ENDRB and PGI-2 synthase), suggesting that 3 integrin signaling could be one of the potential molecular mechanisms behind this genetic reprogramming. v 3 integrin is involved in survival signaling in melanoma cells 21 mediated either through FAK or Shc using the Ras-Raf-MAPK pathway 22,23 as well as PI3K.…”

Section: Discussionmentioning

confidence: 54%

Parallel expression of αIIbβ3 and αvβ3 integrins in human melanoma cells upregulates bFGF expression and promotes their angiogenic phenotype

Döme

Rásó

Dobos

et al. 2005

Intl Journal of Cancer

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Previous studies indicated that transfection of the platelet integrin aIIbb3 into human melanoma cells expressing integrin avb3 promoted their in vivo (but not in vitro) growth and cell survival. To reveal the underlying pathomechanism, we have analyzed the angiogenic phenotype of aIIbb3 integrin-transduced human melanoma cells expressing integrin avb3. Upon heterotopic or orthotopic (intracutaneous) injections into SCID mice, the aIIbb3 integrin-overexpressing clones, ESL, ESH, 19L and 19H, grew more rapidly than the mock transfectant (avb3 expressing) clone, 3.1P. Morphometry demonstrated an increased intratumoral microvessel density in 19L and 19H tumors compared to 3.1P. Immunocytochemistry and flow cytometry indicated that vascular endothelial growth factor (VEGF) is constitutively expressed in the majority of the cells of both the mock and the aIIbb3 integrintransfected clones. However, the mock transfectant clone, 3.1P, did not express basic fibroblast growth factor (bFGF) at protein level (<1%), unlike the aIIbb3 integrin-transfected clones, 19L and 19H, (33.9 and 84.1%, respectively). Quantitative PCR analysis of 6 related human melanoma clones with various levels of aIIbb3 integrin expressions revealed a correlation between the aIIb protein and bFGF mRNA expressions. Furthermore, cDNA microarray analysis of the 19H cells revealed 12 downregulated and 36 upregulated genes [among them 3 upregulated vasculogenic mimicry-genes (CD34, endothelin receptor B, Prostaglandin I-2 synthase)] when compared to 3.1P cells. The altered bFGF expression may be influenced by integrin-linked signaling, since b3-endonexin is upregulated in aIIbb3-transfected cells and tyrosine kinase inhibitors downregulate bFGF both at mRNA and protein levels. We propose here that the illegitimate expression of aIIbb3 integrin in human melanoma cells already expressing avb3 integrin may alter their in vivo growth properties due to the modulation of their angiogenic phenotype. ' 2005 Wiley-Liss, Inc.

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“…Second, CSCs may trans-differentiate into cancer-associated stromal cells [58][59][60][61][62][65][66][67][68][69], such as cancer-associated fibroblasts and tumor endothelial cells [70,71]. The CSC-differentiated tumor endothelial cells are important in tumor neovascularization and the genesis of TME [72][73][74][75]. Third, CSCs release various stem cell factors that induce normal stromal cells to become cancer-associated stromal cells, such as cancer-associated fibroblasts (CAFs) [1] and tumor endothelial cells (TEMs) [76], and to recruit immune cells from bone marrow and blood to the tumor tissue.…”

Section: Cancer Stem Cells and Tumor Microenvironmentmentioning

confidence: 99%

“…3). These tumor cells include precancerous stem cells [59][60][61], CSCs [62][63][64], and vasculogenic tumor cells [71][72][73][74][75].…”

Section: Tumor Neovascularization and Cancer Stem Cell Nichementioning

confidence: 99%

Deciphering the Key Features of Malignant Tumor Microenvironment for Anti-cancer Therapy

Shang

Zhang

Pan

et al. 2012

Cancer Microenvironment

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Tumor microenvironment (TME) is important in tumor development and may be a target for anti-cancer therapy. The genesis of TME is a dynamic process that is regulated by intrinsic and extrinsic factors and coordinated by multiple genes, cells, and signal pathways. Cancer anaerobic metabolism and various oncogenes may stimulate the genesis of TME. Tumor cells and cancer stem cells actively participate in the genesis of the cancer stem cell niche and tumor neovascularization, important in the initiation of the TME. Various cancer-associated stromal cells, derived niche factors, and tumor-associated macrophages may function as promoters in the genesis of the TME. Dicer1 gene-deleted stromal cells can induce generation of cancer stem cells and initiate tumorigenesis, suggesting that stromal cells also may promote the genesis of the TME. Therefore, the key features of TME include niche-driving oncogenes, cancer anaerobic metabolism, niche-driving cancer stem cells, neovascularization, tumor-associated inflammatory cells, and cancer-associated stromal cells. These features are potential targets for normalization of the malignant TME and effective anti-cancer therapy.

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Vasculogenic mimicry and tumour-cell plasticity: lessons from melanoma

Cited by 758 publications

References 91 publications

Metalloproteinases and their inhibitors in tumor angiogenesis

Metalloproteinases and their inhibitors in tumor angiogenesis

Parallel expression of αIIbβ3 and αvβ3 integrins in human melanoma cells upregulates bFGF expression and promotes their angiogenic phenotype

Deciphering the Key Features of Malignant Tumor Microenvironment for Anti-cancer Therapy

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