ETH Zurich researchers reveal how colorectal cancer cells colonise the liver

Bowel cancer, the third most common cancer type worldwide, is the second most common cause of cancer death

Researchers from ETH Zurich, Switzerland, have revealed how colorectal cancer cells colonise the liver, which could help to develop future treatments that can be a hindrance to the formation of often fatal metastases.

The study published in Nature Cell was led by Andreas Moor, an assistant professor in the department of biosystems science and engineering at ETH Zurich.

Currently the third most common cancer type worldwide and the second most common cause of cancer death, colorectal cancer, otherwise known as bowel cancer, occurs when abnormal cells start to divide and grow in an uncontrolled way in the large bowel and back passage.

In most cases of fatal cancer, metastasis is the most likely cause, which occurs when the primary tumour has sent out cells and invaded other organs of the body.

With no current treatment to prevent the metastatic process, researchers tested on genetically modified mice and discovered that a protein called Plexin-B2 and colorectal cancer cells possess certain proteins from the semaphorin family – a large family of secreted and transmembrane proteins that are conserved from invertebrates to mammal – allowing colorectal cancer cells to attach themselves to liver cells.

“Colorectal cancer metastasises to the liver because of how our blood flows,” explained Moor.

In addition, the study shows that colorectal cancer metastasises earlier and more frequently to the liver when the tumour contains large amounts of semaphoring on its surface. When triggered by plexin and semaphorin, colorectal cancer cells begin to change.

In order to break away from the primary tumour, the cancer cells have to change their identity by freeing themselves from the surface layers of the intestine and severing their close connections to neighbouring cells.

Researchers believe that it may be possible to prevent the cancer from establishing new tumours if further research into the interaction between plexin and semaphorin is successful.