Cancer cells remain clumped together via a sort of 'Velcro' which allows them to adhere to each other wherever they appear. In order for cancer cells to leave a tumour and spread throughout the body during metastatic processes, cancer cells must reduce their adhesion and increase their ability to migrate. They can do this by changing the amount and type of proteins on their surface.
The researchers targeted these surface proteins, particularly one called CD166, a kind of microscopic 'Velcro' which allows the cells to stick together.
The researchers observed that certain cancer cells are, in fact, capable of decreasing the abundance of this 'Velcro' (CD166) on their surface. More specifically, these cells have found a way to reduce the adhesion of their surface by redirecting it into small internal vesicles: this is a mechanism called endocytosis, which the researchers highlighted in their study published in the prestigious scientific journal Nature Communications.
The authors show that endophilin-A3—but neither A1 nor A2 isoforms—functionally associates with CD166-containing early endocytic carriers and physically interacts with the cargo. Our data further demonstrates that the three endophilin-A isoforms control the uptake of distinct subsets of cargoes.
In addition, the authors provide strong evidence that the construction of endocytic sites from which CD166 is taken up in an endophilin-A3-dependent manner is driven by extracellular galectin-8.
If there is less adhesion, owing to less 'Velcro' (CD166) on the surface of cancer cells, they stick together less and therefore migrate more easily.
The next step? This fundamental mechanism still has many secrets to reveal. But the researchers hypothesise that it could contribute to the formation of metastases which allow cancer to spread. And who knows, in the future this will perhaps make it possible to develop new solutions that block metastases and thus slow down the development of certain cancers.
Mechanism for cancer cells to detach and migrate
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