Certain cancer cells may use amyloid bodies, characteristic of Alzheimer’s disease, to store proteins while they lie dormant. Breaking these down could reactivate dormant cells and enable better treatment
Amyloid clumps are usually indicative of neurodegenerative disease, and are typically caused by misfolded proteins that begin to stick together – forming sticky, damaging plaques. In an unusual finding, a team of scientists from the Sylvester Comprehensive Cancer Center have discovered that some cancer cells appear to store proteins as similar amyloid bodies while lying dormant.
“The amyloid state of protein organization is typically associated with debilitating human neuropathies and rarely observed in physiology. Yet, we found that a large number of proteins are stored as amyloid bodies in cancer cells that are dormant. The heat shock chaperone pathway can disaggregate the amyloid bodies and turn the dormant cancer cells into active, progressing cancer cells”
A new drug target?
The finding is curious as amyloid bodies are typically detrimental, but in these cells they appear to be used as a storage mechanism instead. When the researchers delved further they found particular signals from ribosomal intergenic noncoding RNA (RNA that doesn’t code for a new protein), were driving this amyloid formation. Furthermore, the heat shock pathway, which is a cellular pathway that responds to misfolded proteins or changes that encourage misfolding (such as temperature rise), appears to unlock these bodies; allowing cancer cells to jolt back into life. This means that we may be able to repurpose drugs currently being researched for Alzheimer’s and disaggregate these bodies in order to wipe out latent cells. We may also be able to manipulate RNA signals to increase these protein stores and turn problem cells in dormant ones.
“If we can stop the amyloid bodies from disaggregating in cancer cells, the hope is that they will remain dormant indefinitely. In addition, we may also be able to turn active cancer cells into dormant ones by encouraging them to store the proteins as amyloid bodies.There are already drugs on the market, and others are being studied, that target the ribosomal intergenic noncoding RNA as well as the heat shock chaperone pathway”
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