Vasculogenic mimicry (VM)

Vasculogenic mimicry refers to a process where aggressive tumor cells create fluid-conducting, vessel-like networks within a tumor without the involvement of endothelial cells, thus mimicking natural vasculature formation[1][2][3][4][5]. This process provides oxygen and nutrients to tumors and removes waste, functioning independently of canonical angiogenesis. VM is associated with cancer cell plasticity, hypoxia adaptation, stem-cell-like features, and epithelial–mesenchymal transition (EMT)[2][3][4]. Molecular mechanisms include aberrant expression of VE-cadherin, activation of matrix metalloproteinases (MMPs), and signaling through EphA2, Notch4, Nodal, VEGFR1, HIFs, and Twist1[2][3][4][6]. VM is predominantly observed in aggressive malignancies and strongly correlates with increased metastasis, poor prognosis, and resistance to conventional anti-angiogenic therapies[1][2][3][4]. PAS+/CD31– staining and molecular markers such as VE-cadherin and laminin-5γ2 are used as biomarkers for VM[1][5][6]. Important Note: Vasculogenic mimicry is not a molecule, gene, or receptor, but a process/phenotype, so it should not be included in databases of molecular drug targets without proper annotation as a phenotypic process.

Other names

Vascular mimicryVM