title: Vasculogenic mimicry and tumor metastasis.
abstract: Vasculogenic mimicry (VM), a microvascular channel made up of nonendothelial cells, has been accepted as a new model of neovascularization in aggressive tumors, owning to the specific capacity of malignant cells to form vessel-like networks which provide sufficient blood supply for tumor growth. Multiple molecular mechanisms, especially vascular endothelial (VE)-cadherin, erythropoietin-producing hepatocellular receptor A2 (EphA2), phosphatidyl inositol 3-kinase (PI3K), matrix metalloproteinases (MMPs), vascular endothelial growth factor receptor (VEGFR1), and hypoxia inducible factor (HIF)-1a, have been reported to participate in VM formation which is associated with tumor migration and invasion. In addition, hypoxia, cancer stem cells (CSCs) and epithelial-mesenehymal transition (EMT) are regarded as significant factors in VM formation and tumor metastasis. Due to the important effects of VM on tumor progression, a review was carried out in the present study, to synthetically analyze the relationship between VM and tumor metastasis.
authors: Department of Graduate, Weifang Medical College, Weifang, Shandong, Chin.
authors: Jingxin
authors: J
authors: Zhang
authors: Lili
authors: L
authors: Qiao
authors: Ning
authors: N
authors: Liang
authors: Jian
authors: J
authors: Xie
authors: Hui
authors: H
authors: Luo
authors: Guodong
authors: G
authors: Deng
authors: Jiandong
authors: J
authors: Zhang
mesh_terms: D054337:Cell Dedifferentiation; D058750:Epithelial-Mesenchymal Transition; D006801:Humans; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000098:blood supply*; D014411:Neoplastic Stem Cells / Q000502:physiology; D009389:Neovascularization, Pathologic / Q000209:etiology*