Research reveals how the body can detect cancerous cells

Image Credit: NASA’s Marshall Space Flight Center via Flickr

Cancer is a group of diseases characterised by excessive cell division due to DNA damage, and can afflict many different cell types. Mutations often arise in genes involved in cell growth and survival, which makes cancer difficult to target and treat. However, the field of cancer therapy is moving forward at a swift pace, thanks to cutting-edge research into the processes and mechanisms that promote cancer development. 

A recent University of Edinburgh study has identified an important control mechanism in the immune response against cancer: a molecule called TLR2. TLR2 is located on the surface of cells and recognises molecular patterns from invading microbes and damaged cells. It can then activate an innate immune response to promote the destruction of microorganisms or damaged cells to protect against disease and cancer. This study has shown that the body can harness a process known as senescence, normally used to clear old or dying cells, to sense cells that are damaged and may become cancerous. Senescence can be induced by cell stress, such as the activation of cancer-causing genes (oncogenes), and halts cell division to prevent damaged cells proliferating out of control. This process also causes inflammation – most of us will be familiar with the swelling and redness typical of an inflamed injury. These symptoms are caused by the release of inflammatory molecules to attract immune cells to the site of injury. A similar mechanism is occurs in senescence. Proinflammatory molecules, known as the senescence-associated secretory phenotype, are produced, activating an immune response to clear the senescent cells. This provides a means for controlling tumour development. It is this process that the researchers focussed on, in an effort to reveal the way in which the body can sense cancer cells.

The researchers used cells with an inducible cancer gene to study the mechanisms of TLR2 in cancer cell senescence. They found that TLR2 interacted with a similar molecule, TLR10 and both were essential for the production of proinflammatory molecules, without which the process was blocked. It was discovered that TLR2 activated genes involved in stopping cell division, and therefore prevents the continued growth of cancerous cells. The researchers also uncovered an important feedback loop: the production of inflammatory molecules increases TLR2 activity, which, in turn, leads to more inflammation. This loop amplifies the message, stimulating the termination of cancerous cells by the immune system. These observations of cancer cell clearance may open up new possibilities in cancer treatment. The ability to target these pathways with genetic modification or new medicines could allow us to mobilise the body’s own processes to target the disease in its early stages.

Understanding the fine detail of the molecular interactions involved in cancer development is important for developing novel therapies against this ever-evolving group of diseases. This study provides an exciting insight into how the body can control and prevent tumour development, and these processes have the potential to be harnessed for therapeutic purposes. 

This article was written by Eilidh Vandome and edited by Miles Martin

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