Overview of advances in vasculogenic mimicry – a potential target for tumor therapy

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Abstract

Vasculogenic mimicry (VM) describes the process utilized by highly aggressive cancer cells to generate vascular-like structures without the presence of endothelial cells. VM has been vividly described in various tumors and participates in cancer progression dissemination and metastasis. Diverse molecular mechanisms and signaling pathways are involved in VM formation. Furthermore, the patterning characteristics of VM, detected with molecular imaging, are being investigated for use as a tool to aid clinical practice. This review explores the most recent studies investigating the role of VM in tumor induction. Indeed, the recognition of these advances will increasingly affect the development of novel therapeutic target strategies for VM in human cancer.

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Vascular channel formation by human melanoma cells in vivo and in vitro: vasculogenic mimicry.

A. Maniotis, R Folberg, A. Hess … (1999)

Tissue sections from aggressive human intraocular (uveal) and metastatic cutaneous melanomas generally lack evidence of significant necrosis and contain patterned networks of interconnected loops of extracellular matrix. The matrix that forms these loops or networks may be solid or hollow. Red blood cells have been detected within the hollow channel components of this patterned matrix histologically, and these vascular channel networks have been detected in human tumors angiographically. Endothelial cells were not identified within these matrix-embedded channels by light microscopy, by transmission electron microscopy, or by using an immunohistochemical panel of endothelial cell markers (Factor VIII-related antigen, Ulex, CD31, CD34, and KDR[Flk-1]). Highly invasive primary and metastatic human melanoma cells formed patterned solid and hollow matrix channels (seen in tissue sections of aggressive primary and metastatic human melanomas) in three-dimensional cultures containing Matrigel or dilute Type I collagen, without endothelial cells or fibroblasts. These tumor cell-generated patterned channels conducted dye, highlighting looping patterns visualized angiographically in human tumors. Neither normal melanocytes nor poorly invasive melanoma cells generated these patterned channels in vitro under identical culture conditions, even after the addition of conditioned medium from metastatic pattern-forming melanoma cells, soluble growth factors, or regimes of hypoxia. Highly invasive and metastatic human melanoma cells, but not poorly invasive melanoma cells, contracted and remodeled floating hydrated gels, providing a biomechanical explanation for the generation of microvessels in vitro. cDNA microarray analysis of highly invasive versus poorly invasive melanoma tumor cells confirmed a genetic reversion to a pluripotent embryonic-like genotype in the highly aggressive melanoma cells. These observations strongly suggest that aggressive melanoma cells may generate vascular channels that facilitate tumor perfusion independent of tumor angiogenesis.

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A new alternative mechanism in glioblastoma vascularization: tubular vasculogenic mimicry.

Soufiane El Hallani, Carole Colin, Marc Sanson … (2010)

Glioblastoma is one of the most angiogenic human tumours and endothelial proliferation is a hallmark of the disease. A better understanding of glioblastoma vasculature is needed to optimize anti-angiogenic therapy that has shown a high but transient efficacy. We analysed human glioblastoma tissues and found non-endothelial cell-lined blood vessels that were formed by tumour cells (vasculogenic mimicry of the tubular type). We hypothesized that CD133+ glioblastoma cells presenting stem-cell properties may express pro-vascular molecules allowing them to form blood vessels de novo. We demonstrated in vitro that glioblastoma stem-like cells were capable of vasculogenesis and endothelium-associated genes expression. Moreover, a fraction of these glioblastoma stem-like cells could transdifferentiate into vascular smooth muscle-like cells. We describe here a new mechanism of alternative glioblastoma vascularization and open a new perspective for the antivascular treatment strategy.

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Tumor cell vasculogenic mimicry: from controversy to therapeutic promise.

Richard Seftor, Angela Hess, Elisabeth Seftor … (2012)

In 1999, The American Journal of Pathology published an article entitled "Vascular channel formation by human melanoma cells in vivo and in vitro: vasculogenic mimicry," by Maniotis and colleagues, which ignited a spirited debate for several years and earned distinction as a citation classic. Tumor cell vasculogenic mimicry (VM) refers to the plasticity of aggressive cancer cells forming de novo vascular networks, which thereby contribute to perfusion of rapidly growing tumors, transporting fluid from leaky vessels, and/or connecting with the constitutional endothelial-lined vasculature. The tumor cells capable of VM share a plastic, transendothelial phenotype, which may be induced by hypoxia. Since VM was introduced as a novel paradigm for melanoma tumor perfusion, many studies have contributed new findings illuminating the underlying molecular pathways supporting VM in a variety of tumors, including carcinomas, sarcomas, glioblastomas, astrocytomas, and melanomas. Facilitating the functional plasticity of tumor cell VM are key proteins associated with vascular, stem cell, and hypoxia-related signaling pathways, each deserving serious consideration as potential therapeutic targets and diagnostic indicators of the aggressive, metastatic phenotype. Copyright © 2012 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.

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Author and article information

Journal

Journal ID (nlm-ta): Cancer Manag Res

Journal ID (iso-abbrev): Cancer Manag Res

Journal ID (publisher-id): Cancer Management and Research

Title: Cancer Management and Research

Publisher: Dove Medical Press

ISSN (Electronic): 1179-1322

Publication date Collection: 2018

Publication date (Electronic): 02 August 2018

Volume: 10

Pages: 2429-2437

Affiliations

[1 ]Department of Radiation Oncology, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, People’s Republic of China, gehong616@ 123456126.com

[2 ]Division of Graduate, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, People’s Republic of China

Author notes

Correspondence: Hong Ge, Department of Radiation Oncology, The Affiliated Cancer Hospital of Zhengzhou University, No. 127 Dongming Road, Zhengzhou 450008, Henan Province, People’s Republic of China, Tel +86 371 6558 7765, Fax +86 371 6558 7713, Email gehong616@ 123456126.com

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Publisher ID: cmar-10-2429

DOI: 10.2147/CMAR.S164675

PMC ID: 6080880

PubMed ID: 30122992

SO-VID: a8644753-f07b-4932-9ed8-d28dc153539f

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The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

Overview of advances in vasculogenic mimicry – a potential target for tumor therapy

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Most cited references 80

Vascular channel formation by human melanoma cells in vivo and in vitro: vasculogenic mimicry.

A new alternative mechanism in glioblastoma vascularization: tubular vasculogenic mimicry.

Tumor cell vasculogenic mimicry: from controversy to therapeutic promise.

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