Vasohibin-Mediated Angiogenesis Regulation in Cancer Systems
Summary
The vasohibin family of regulatory proteins comprises two isoforms with opposing functions in angiogenesis. VASH1, primarily secreted by endothelial cells, acts as an autocrine inhibitor, limiting pathological vessel sprouting and reinforcing vascular stability. Conversely, VASH2 is expressed by tumour cells and drives neovascularisation to sustain malignant growth. This yin–yang balance influences blood flow, vessel maturity and permeability within the tumour microenvironment, thereby modulating hypoxia, immune cell infiltration and response to chemotherapy. At the molecular level, vasohibins exert effects through enzymatic activity linked to a non-canonical protease catalytic triad, interaction with extracellular matrix receptors, and transcriptional networks governing junctional proteins. Dysregulation of these pathways contributes to uncontrolled vessel formation, enhanced metastatic potential and resistance to cytotoxic agents. Understanding vasohibin-mediated signalling offers therapeutic avenues, including design of selective inhibitors or enhancers to normalise tumour vasculature, improve drug delivery and restrain tumour progression across diverse cancer types.
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Vasohibin-Mediated Angiogenesis Regulation in Cancer Systems publication trend
The graph below shows the total number of articles in vasohibin-mediated angiogenesis regulation in cancer systems across all publications each year (not limited to Nature Index journals).
Technical terms
Angiogenesis: Formation of new blood vessels from pre-existing vasculature.
Vasohibin-1 (VASH1): Endogenous endothelial factor that inhibits vessel sprouting and stabilises vessel walls.
Vasohibin-2 (VASH2): Tumour-derived protein that promotes angiogenesis and supports tumour expansion.
Tumour microenvironment: Cellular, molecular and structural milieu surrounding a tumour, including blood vessels, immune cells and matrix components.
Epithelial–mesenchymal transition (EMT): Cellular programme enabling epithelial cells to adopt mesenchymal characteristics, facilitating invasion and metastasis.
Catalytic triad: Three amino acid residues in proteases that cooperate to cleave peptide bonds.
Ribonucleotide reductase regulatory subunit M2 (RRM2): Enzyme subunit essential for deoxyribonucleotide synthesis and DNA replication, often upregulated in cancer.
References
- Revealing the inhibitory effect of VASH1 on ovarian cancer from multiple perspectives. Cancer Biology & Therapy (2023).
- Vasohibins: new transglutaminase-like cysteine proteases possessing a non-canonical Cys-His-Ser catalytic triad. Bioinformatics (2016).
- Vasohibin 2 reduces chemosensitivity to gemcitabine in pancreatic cancer cells via Jun proto-oncogene dependent transactivation of ribonucleotide reductase regulatory subunit M2. Molecular Cancer (2017).
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