The protein plaques that build up in the brains of Alzheimer’s sufferers can also develop in cancer cells, causing them to become dormant. Armed with this knowledge, researchers are now hopeful of devising new treatments that may be able to stop cancer in its tracks.
Reporting their discovery in the journal Developmental Cell, the study authors explain that when cells are placed under highly stressful conditions – such as high temperatures or a lack of oxygen – they strategically shut down their major processes in order to avoid malfunctioning. One of the ways in which they achieve this is by immobilizing certain proteins that normally move freely through the cell in order to execute a range of functions.
In Alzheimer’s, some proteins become joined together to form aggregations called amyloids, which are toxic to neurons. Because most proteins have the ability to join these amyloids, the researchers hypothesized that they may also form elsewhere in the body, serving a beneficial purpose by locking cellular proteins together and immobilizing them when cells need to temporarily shut down.
To test this, they placed cells in a hypoxic environment – meaning a lack of oxygen – and used a special dye to indicate the presence of amyloids. They discovered that hypoxia did indeed lead to the formation of amyloids, and that once oxygen levels returned to normal, these amyloids disappeared.
The blue dots incise these cells are amyloid plaques. Sylvester Comprehensive Cancer Center
From this, they were able to conclude that the formation of amyloids plays a key role in halting cellular function under stress, and that this process is reversible. They also found that both the formation and dissolution of amyloids is mediated by a type of genetic material known as non-coding RNA.
Given that hypoxia has previously been associated with cancer cell dormancy, the team decided to repeat the experiment using human cancer cells, and found that once again, amyloids appear when oxygen is low, causing cells to stop dividing, and later dissolve when conditions return to normal, freeing up individual proteins and enabling the cancer to continue developing.
In a statement, study co-author Stephen Lee explained that “if we can stop the amyloid bodies from disaggregating in cancer cells, the hope is that they will remain dormant indefinitely.” Alternatively, he says “we may also be able to turn active cancer cells into dormant ones by encouraging them to store the proteins as amyloid bodies.”
Doing so may depend on the development of medications that target the relevant non-coding RNA, causing the formation of amyloids. Fortunately, Lee says that there are already a number of drugs in development that could potentially act on this pathway.
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