Researchers at Okayama University describe in the journal Scientific Reports the role of an extracellular protein, versican, in regulating tumour growth and providing a newly formed network of blood vessels to further nourish the tumour.

Angiogenesis is the creation of new blood vessels from the branching of pre-existing ones.

This phenomenon is especially important in the context of cancer, because it supplies the tumours with additional oxygen and nutrients to keep them growing.

An effective strategy in treating cancer would therefore be to prevent angiogenesis.

However, factors in the tumour microenvironment that may boost angiogenesis are still poorly understood.

The tumour microenvironment, is a mix of host tissue (stroma) and tumour cells. 

A recent study in Scientific Reports by Professor Satoshi Hirohata et al. has found a link between angiogenesis and the tumour microenvironment, in the form of an extracellular matrix protein called versican.

Versican is involved in several vascular processes, but its role regarding tumour angiogenesis isn’t well understood.

Professor Hirohata and his team members at Okayama University looked at different cancer cells lines, and found that although initially they all had varying amounts of versican, tumours derived from all the cell lines had amplified quantities of the protein.

Using a technique called Western blotting, they showed that a melanoma producing cell line B16F10, had very low levels of versican which increased drastically after tumour initiation, while a lung cancer cell line (LLC) had high levels of versican before tumour induction, which were even more pronounced after.

Interestingly, it was found that all the tumours had versican which was at least partly derived from the stromal microenvironment.

After establishing the origins of tumour versican, the researchers noticed that versican was located in the vicinity of blood vessels, within tumours.

It was also stationed specifically with macrophages (safe-guarding cells in the blood), suggesting that stromal macrophages might be producing it. Versican present in tumours was not in its complete form, but a smaller cleaved form, which is easily distinguishable from normal versican.

Finally, to see the direct effects of versican on tumour angiogenesis, the researchers compared two B16F10 genetic variants of mice: one that inherently produced versican, and one that could not.

The latter had smaller tumour size and fewer blood vessels, strongly suggesting a firsthand involvement of versican with tumour angiogenesis.

This study has found yet another remarkable way in which cancer cells exploit host tissues to proliferate.

“Our findings suggest that versican is an intriguing target to consider in combating tumour growth and angiogenesis”, conclude the authors.

Source: Okayama University