New research hints at why some cancer cells develop drug resistance, and how to kill them.
As with weeds in a garden, it is a challenge to fully get rid of cancer cells in the body once they arise. They have a relentless need to continuously expand, even when they are significantly cut back by therapy or surgery. Even a few cancer cells can give rise to new colonies that will eventually outgrow their borders and deplete their local resources.
We are researchers studying how these microenvironmental stresses affect tumor initiation and progression. In our new study , we found that the harsh microenvironments of the body can push certain cancer cells to overcome the stress of being isolated and make them more adept at initiating and forming new tumor colonies.
We found that pancreatic cancer cells challenged with conditions that mimic isolation stress gain a new receptor on their surface that unstressed cancer cells don’t typically have: lysophosphatidic acid receptor 4, or LPAR4 , a protein involved in tumor progression. We determined that a key component of this extracellular matrix is fibronectin . When this protein binds to receptors called integrins on the surface of cells, it triggers a cascade of events that results in the expression of new genes promoting tumor initiation, stress tolerance and cancer progression. Eventually, other cancer cells are recruited into the fibronectin-rich matrix network, and a new satellite tumor colony starts to form.
Keeping cancer cells stressedUnderstanding how to cut off the cascade of events that allows cancer cells to become stress-tolerant is important, because it provides a new area to explore for future treatments.
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