Angiogenesis in Hepatocellular Carcinoma
Summary
Angiogenesis, the process by which new blood vessels sprout from existing vasculature, is a hallmark of hepatocellular carcinoma (HCC). Tumour cells exploit this mechanism to secure oxygen and nutrients, supporting rapid proliferation and facilitating metastasis. Key molecular drivers include hypoxia‐inducible factors (notably HIF-1α) that transcriptionally activate vascular endothelial growth factor (VEGF) and other pro-angiogenic mediators. The tumour microenvironment, comprising endothelial cells, pericytes, immune populations and the extracellular matrix, orchestrates a dynamic interplay that can promote aberrant vessel formation, vessel co-option or vascular mimicry. Clinically, anti-angiogenic therapies—such as multi-kinase inhibitors—have extended survival in advanced HCC, yet resistance often emerges through compensatory pathways. Understanding the balance between pro- and anti-angiogenic signals, and how they intersect with metabolic reprogramming, immune suppression and mechanical remodelling, is essential for devising more durable interventions and personalising treatment strategies.
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Angiogenesis in Hepatocellular Carcinoma publication trend
The graph below shows the total number of articles in angiogenesis in hepatocellular carcinoma across all publications each year (not limited to Nature Index journals).
Technical terms
Angiogenesis: The formation of new blood vessels from pre-existing vasculature.
Tumour microenvironment: The cellular and non-cellular milieu, including immune cells, blood vessels and extracellular matrix, surrounding tumour cells.
Hypoxia-inducible factor-1α (HIF-1α): A transcription factor stabilised under low oxygen that upregulates genes involved in angiogenesis and metabolism.
Vascular endothelial growth factor (VEGF): A family of signalling proteins that stimulate endothelial cell proliferation and new vessel formation.
Transarterial chemoembolization (TACE): A locoregional procedure delivering chemotherapy and embolic agents directly to tumour vasculature to induce ischemia.
Glutamine transporter SLC1A5: A membrane protein facilitating glutamine uptake, implicated in metabolic regulation of tumour angiogenesis and therapy resistance.
Ubiquitin-proteasome pathway: The cellular mechanism for protein degradation, tagging substrates with ubiquitin for proteasomal breakdown.
References
- In vitro integration of a functional vasculature to model endothelial regulation of chemotherapy and T-cell immunotherapy in liver cancer. Biomaterials (2025).
- Elevated SLC1A5 associated with poor prognosis and therapeutic resistance to transarterial chemoembolization in hepatocellular carcinoma. Journal of Translational Medicine (2024).
- TRIM55 restricts the progression of hepatocellular carcinoma through ubiquitin-proteasome-mediated degradation of NF90. Cell Death Discovery (2024).
- The Changes of HIF-1α and VEGF Expression After TACE in Patients With Hepatocellular Carcinoma. Journal of Clinical Medicine Research (2016).
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