Does Cancer Metastasis Occur via a Quorum-Sensing-Like Mechanism?

 

Does Cancer Metastasis Occur via a Quorum-Sensing-Like Mechanism?

 

In February, The Hindu published an article titled “Bacteria Can Talk to Each Other and Are Multilingual, Says Biologist.” The biologist in question is Bonnie Bassler, who runs a laboratory at Princeton University and has spent her career studying a process called quorum sensing in bacteria. Quorum sensing is the mechanism by which bacteria communicate and coordinate group behavior based on population density. They do this by continuously secreting and detecting chemical signaling molecules known as autoinducers. Once the bacterial population reaches a critical threshold, the resulting concentration of autoinducers triggers the synchronized activation of specific genes.

After listening to a conversation with Bassler on physicist Sean Carroll's podcast, Mindscape, I found myself wondering whether metastasis — the spread of cancer to distant organs — might occur through a similar, quorum-sensing-like mechanism.

Metastasis involves a step called the epithelial-to-mesenchymal transition (EMT), in which stationary, polarized epithelial cells lose their cell-to-cell adhesion and acquire migratory, invasive properties, becoming mesenchymal cells. This same process also plays a crucial role in embryonic development and wound healing. Within the primary tumor, cells proliferate uncontrollably and secrete enzymes called matrix metalloproteinases (MMPs), such as MMP2 and MMP9. These enzymes initiate and sustain EMT by breaking down basement membranes, degrading adhesion molecules like E-cadherin, and releasing pro-EMT signaling factors such as TGF-β from the extracellular matrix. Together, these actions drive cancer invasion and metastasis.

If quorum sensing is indeed involved in EMT, it may work as follows: in the primary tumor, cells divide uncontrollably and release MMPs, which act much like autoinducers. As the tumor cells multiply, MMP concentration rises in step with them, and once the tumor reaches a critical size, this rising concentration of MMPs triggers the synchronized activation of EMT genes. This remains a hypothesis, however, and would need to be tested directly in primary tumor cells through wet-lab experiments in tissue culture.