Research progress on vasculogenic mimicry in colorectal cancer: mechanisms and therapeutic

Colorectal cancer (CRC) is the third most common malignant tumor worldwide and is characterized by high incidence and mortality rates. In the chemotherapeutic treatment of CRC, antiangiogenic therapy is utilized throughout the entire disease course, particularly for highly metastatic tumors. However, studies have reported that resistance to current antiangiogenic therapies often develops, leading to suboptimal clinical outcomes. Vasculogenic mimicry (VM) represents a novel tumor blood supply mechanism that is distinct from traditional endothelial cell-dependent vasculature. VM channels are composed solely of tumor cells and extracellular basement membranes, emerge within malignant tumors requiring blood perfusion, and have been identified in numerous solid tumors. Research indicates that tumors exhibiting VM demonstrate greater proliferative, invasive, and metastatic potential, along with poorer prognosis, than those without VM. Additionally, studies suggest that VM contributes to the limited efficacy and resistance observed with antiangiogenic drugs in clinical practice. Thus, targeting VM is crucial in oncology, especially in CRC. Recent advances have been made in anti-VM drug therapy for CRC. Moving forward, combining VM-targeted strategies with conventional antiangiogenic therapies targeting endothelial cells may represent a promising new direction in CRC treatment. This review summarizes current insights into the mechanisms of VM in CRC and its therapeutic advancements, aiming to provide novel perspectives for clinical management.