Angiogenesis in Cancer

The survival of cancer cells critically depends on vasculature and blood supply which provide essential nutrients and oxygen to support the typically accelerated tumor growth. Additionally, vascular structures (e.g., new vessels, pre-existing vessels and vessel-like structures) allow cancer cells to travel to distant tissues and organs supporting cancer spread. Formation of new vasculature, or angiogenesis, is therefore a process that contributes to tumor growth and metastasis and is particularly critical for solid tumors.

“Angiogenic switch” refers to the activation of molecular pathways that direct the formation of new vessels within a tumor. Specific genetic changes in tumor cells underscore the activation of angiogenic programs by tilting the balance between the activity of angiogenic activators and inhibitors.

Within the angiogenesis cascade, different molecular factors play key roles in the establishment of new vessels. For example, VEGF is a critical angiogenic growth factor which stimulates the proliferation and survival of endothelial cells. In the tumor microenvironment, VEGF expression may be stimulated by hypoxia via the stabilization and activity of HIF transcription factors. Release of VEGF stimulates the concomitant secretion of proteases (e.g., Metalloproteinases- MMP-9) by endothelial cells of mature vessels which degrade the extracellular basement membrane and facilitate the movement and proliferation of endothelial cells. Under the influence of VEGF and other growth factors as well as adhesion molecules (e.g., Integrins) endothelial cells proliferate and migrate to give rise to new vessels.

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