AI Article Synopsis
- - The study identifies a specific change in mammary carcinoma cells that enhances their ability to migrate and metastasize when they experience cell damage, particularly from radiation exposure.
- - This change is linked to increased levels of the gene product cyclooxygenase 2 (Cox2) and its lipid product prostaglandin E2 (PGE2), which activate the PGE2 receptor EP4.
- - Although the enhanced migratory and metastatic properties are temporary, they can be sustained with continued cell damage, and the use of blockers for Cox2 or the PGE2 receptor can prevent this aggressive behavior, suggesting new ways to improve treatment with radiation.
Article Abstract
We describe a cell damage-induced phenotype in mammary carcinoma cells involving acquisition of enhanced migratory and metastatic properties. Induction of this state by radiation required increased activity of the Ptgs2 gene product cyclooxygenase 2 (Cox2), secretion of its bioactive lipid product prostaglandin E2 (PGE2), and the activity of the PGE2 receptor EP4. Although largely transient, decaying to low levels in a few days to a week, this phenotype was cumulative with damage and levels of cell markers Sca-1 and ALDH1 increased with treatment dose. The Sca-1 , metastatic phenotype was inhibited by both Cox2 inhibitors and PGE2 receptor antagonists, suggesting novel approaches to radiosensitization.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6068352 | PMC |
| http://dx.doi.org/10.1002/1878-0261.12321 | DOI Listing |
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